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***THE MAIN BOARDS - Welcome to the Prison Planet Educational Forum and Library*** => PhD Investigative Reports (only for the hardcore) => : Anti_Illuminati October 31, 2009, 01:26:21 AM

: J. Taubenberger & T. Tumpey=BIOTERRORISTS-vaccine+chemtrail Bioweapon
: Anti_Illuminati October 31, 2009, 01:26:21 AM;310/5745/28

Science 7 October 2005:
Vol. 310. no. 5745, pp. 28 - 29
DOI: 10.1126/science.310.5745.28

News of the Week
Resurrected Influenza Virus Yields Secrets of Deadly 1918 Pandemic
Jocelyn Kaiser

As worries about a new flu pandemic mount, researchers have figured out the traits that made the 1918 influenza virus, which killed between 20 million and 50 million people, so virulent. Although a study on page 77 of this issue of Science sheds new light on these questions, it raises a host of others because the researchers reconstructed the complete virus, which no longer existed anywhere on Earth.

Science 7 October 2005:
Vol. 310. no. 5745, pp. 77 - 80
DOI: 10.1126/science.1119392
Prev | Table of Contents | Next
Research Articles
Characterization of the Reconstructed 1918 Spanish Influenza Pandemic Virus
Terrence M. Tumpey,1* Christopher F. Basler,2 Patricia V. Aguilar,2 Hui Zeng,1 Alicia Solórzano,2 David E. Swayne,4 Nancy J. Cox,1 Jacqueline M. Katz,1 Jeffery K. Taubenberger,3 Peter Palese,2 Adolfo García-Sastre2

The pandemic influenza virus of 1918–1919 killed an estimated 20 to 50 million people worldwide. With the recent availability of the complete 1918 influenza virus coding sequence, we used reverse genetics to generate an influenza virus bearing all eight gene segments of the pandemic virus to study the properties associated with its extraordinary virulence. In stark contrast to contemporary human influenza H1N1 viruses, the 1918 pandemic virus had the ability to replicate in the absence of trypsin, caused death in mice and embryonated chicken eggs, and displayed a high-growth phenotype in human bronchial epithelial cells. Moreover, the coordinated expression of the 1918 virus genes most certainly confers the unique high-virulence phenotype observed with this pandemic virus.

1 Influenza Branch, Mailstop G-16, Division of Viral and Rickettsial Diseases (DVRD), National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, NE, Atlanta, GA 30333, USA.
2 Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029, USA.
3 Department of Molecular Pathology, Armed Forces Institute of Pathology, Rockville, MD 20850, USA.
4 Southeast Poultry Research Laboratory, Agricultural Research Laboratory (ARS), U.S. Department of Agriculture (USDA), 934 College Station Road, Athens, GA 30606, USA.

Note added in proof: This research was done by staff taking antiviral prophylaxis and using stringent biosafety precautions (15) to protect the researchers, the environment, and the public. The fundamental purpose of this work was to provide information critical to protect public health and to develop measures effective against future influenza pandemics.

Science 7 October 2005:
Vol. 310. no. 5745, p. 17
DOI: 10.1126/science.310.5745.17
Prev | Table of Contents | Next
1918 Flu and Responsible Science
Phillip A. Sharp*

The influenza pandemic of 1918 is estimated to have caused 50 million deaths worldwide; 675,000 in the United States. The reconstruction of the 1918 virus by the synthesis of all eight subunits and the generation of infectious virus are described on p. 77 of this issue,* and the sequences of the final three gene segments of the virus are described in a concurrent Nature paper. Predictably, but alarmingly, this virus is more lethal to mice than are other influenza strains, suggesting that this property of the 1918 virus has been recovered in the published sequence. The good news is that we now have the sequence of this virus, perhaps permitting the development of new therapies and vaccines to protect against another such pandemic. The concern is that a terrorist group or a careless investigator could convert this new knowledge into another pandemic.

Should the sequence of the 1918 virus have been published, given its potential use by terrorists? The dual-use nature of biological information has been debated widely since September 11, 2001. In 2003, a committee of the U.S. National Academies chaired by Gerald Fink considered this issue, weighing the benefits against the risks of restricting the publication of such biological information.

They outlined the tradeoff between erring on the side of prudence, thus potentially hindering the progress of critical science, and erring on the side of disclosure, thus potentially aiding terrorists. The U.S. National Science Advisory Board for Biosecurity (NSABB) was established to advise governmental agencies and the scientific community on policies relative to public disclosure. This board has begun to deliberate, but the questions are complex, as typified by these papers on the 1918 virus. It is reassuring that the NSABB was asked to consider these papers before publication and concluded that the scientific benefit of the future use of this information far outweighs the potential risk of misuse. People may be reassured that the system is working, because agencies representing the public, the scientific community, and the publishing journals were involved in the decision.


I firmly believe that allowing the publication of this information was the correct decision in terms of both national security and public health. It is impossible to forecast how scientific observations might stimulate others to create new treatments or procedures to control future pandemics. For example, in the Nature article, sequence comparisons suggest that the 1918 virus was generated not by incremental changes in the polymerase genes, but by the movement of these genes, in total, from an avian source into a human influenza virus. The availability of these sequences will permit identification of their avian origin and should show why this particular set of genes was selected. Similarly, the results in the Science article suggest that the cleavage of a protein on the surface of the 1918 virus, a step critical for virulent infection, may occur by a previously unknown mechanism--a hint that could lead to new drugs for inhibiting this step and thus preventing future pandemic eruptions.

Influenza is highly infectious, and a new strain could spread around the world in a matter of months, if not weeks. The public needs confidence that the 1918 virus will not escape from research labs. All of the described experiments were done in a Biosafety Level 3 laboratory, a high-containment environment recommended by the U.S. Centers for Disease Control and Prevention and the National Institutes of Health on an interim basis, whose use should become a permanent requirement for such experiments. Current evidence suggests that some available drugs and possible future vaccines could suppress infections by the 1918 virus. Given the prospect of another natural influenza pandemic, the recent decision by the U.S. administration to stockpile antivirals for influenza treatment seems wise.

Finally, although a sequence of the 1918 virus has been determined and is highly virulent in mice, this may not be the specific form of the virus that caused the pandemic of 1918. An article in the same issue of Nature reports the existence of sequence variation in a natural population of influenza virus; yet we have only one sequence for the 1918 pandemic strain, and the reconstructed virus described in the Science article was built into the backbone of a laboratory strain. Because a pandemic infection is dependent on many unknown properties, there is no certainty that the reconstructed 1918 virus is capable of causing a pandemic.


*T. M. Tumpey et al., Science 310, 77 (2005). J. Taubenberger et al., Nature 437, 889 (2005). S. Salzberg, Nature 10.1038/nature04239 (2005).
Phillip A. Sharp is Institute Professor at the Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.

The 2009 “Novel” Flu Virus was laboratory developed and constructed dating back to approximately 1997, with preliminary recombinant viral research dating back even further. This is the core of the issue (along with the intention to do grievous bodily harm and depraved indifference).

We have numerous related sites with substantial information that the gene splicing and sequencing of this virus has been in operation for at least several years.

Some of the information that provides data on this research follows:

1) GenBank sequences from pandemic (H1N1) 2009 viruses

2) Characterization of the reconstructed 1918 Spanish influenza pandemic virus.

3) Phylogenetic evidence against evolutionary stasis and natural abiotic reservoirs of influenza A virus.

4) Attachment of infectious influenza A viruses of various subtypes to live mammalian and avian cells as measured by flow cytometry.

5) The virulence of the 1918 pandemic influenza virus: unraveling the enigma.

The initial venture was (and most likely still is), funded and/or controlled, directly or indirectly, by the Dept. of Defense, Army Medical Research Institute of Infectious Diseases at Ft. Detrick, MD or their agents.

We know that two individuals, T. Tumpey and J. Taubenberger had cooperated together, via Ft. Detrick, to reverse engineer the 1918 flu virus, and then to recombine these 1918 flu virus genetic sequences with avian and swine flu viral pathogens, creating an entirely new, “Novel” flu virus.

The following information provides insights into this development:

1) Experimental infection of pigs with the human 1918 pandemic influenza virus.

2) The influenza viruses (and avian pathogen experiments)

3) Global host immune response: pathogenesis and transcriptional profiling of type A influenza viruses expressing the hemagglutinin and neuraminidase genes from the 1918 pandemic virus.
Kash JC, Basler CF, García-Sastre A, Carter V, Billharz R, Swayne DE, Przygodzki RM, Taubenberger JK, Katze MG, Tumpey TM.

After completing the reverse engineered “Novel” virus, the creators and associated scientists then set out to work on a vaccine. Some had gone to the National Institutes of Health, and worked in concert with some of the pharmaceutical firms, including Novartis and others.

We also know that in 1987, a corporation named, Novavax, was created specifically for the development of recombinant vaccine research. As such, following their work at NIH and Ft. Detrick, Tumpey and Taubenberger consulted for Novavax as well as Novartis, since they now had completed their the gene sequencing (rRNA) work for the new pandemic flu virus, and its subsequent release by government operatives.

This work clearly shows its intended target is the human population…

1) Show recombinant needed for specific human host.

Attachment of infectious influenza A viruses of various subtypes to live mammalian and avian cells as measured by flow cytometry.

2) Recent avian H5N1 viruses exhibit increased propensity for acquiring human receptor specificity.

3) Recent changes among human influenza viruses.

Currently, from information gathered, it would appear that Novartis, receiving huge amounts of funding from government sources, had patented its current untested and potentially dangerous, squalene-based flu vaccines. ( Provisional Application No. 60/734,026 dtd. Nov. 4, 2005 and P.A. No. 60/812,475 dtd. June 8, 2006: Publication No. US2009/0047353 A1 ).

Novartis, has apparently offered members of the pharmaceutical cartel “vaccine kits” for a fee, to subcontract out additional manufacture of their patented (deadly) vaccine, including Baxter, and several others.


It should also be noted, that between 1997, (when this work at Ft. Detrick began), and 2006, we have traced the “unsolved” murders of at least 20 scientists, microbiologists, and others, that were associated with this research.

My investigative insights and the collateral information seems to indicate that this is (one facet) of a multi-national criminal enterprise of epic proportions. Therefore, I believe the criminal investigation should be handled, in two parts.

The first part should be handled at the U.S. and domestic level, regarding the flu virus manufacture and the toxic vaccine development within the United States. The evidence presented would first go to a U.S. Attorney for the convening of a grand jury.

The second aspect, is an international investigation by respective countries and their Ministries of Justice, or Interpol, and eventually, charges might be brought before the International Court - The Hague or the host country where the criminal act(s) occurred.

The inter-connections and complexity of this case may not have any precedent; therefore, new legal ground may need to “broken”.

It would be a grave injustice to humanity if this is allowed to get “lost in the quagmire”. Only we, the people, can ensure that it does not, and that justice is served for the criminal recombinant virus, the intentional virus’ release, its deadly vaccines, and the deaths and disabilities resulting from these.

The murders of the associated scientists who had worked on parts of this project, would be another matter to contend with. We certainly have motive, and the government or high-priced drug firms can create the opportunity and the means. This, of course will require further exploration, and may be revealed in the ongoing virus investigations with any luck.

It is equally our hope to assemble and develop a palatable array of criminal charges to be brought before the U.S. Attorney’s office. A U.S. Attorney with the moral fiber and intestinal fortitude to see that justice is, indeed accomplished, and the guilty parties,
agencies, and other co-conspirators are prosecuted to the fullest extent of the law.


Dr. Evangelista explains that, “it is necessary to expose and criminally charge the culpable parties that are responsible for the original virus, itself”, and this is where the “bear sits in the buckwheat”. This is the point where things began…the point of origin.

We also can include the toxic vaccine development, and expose the actual individuals that have perpetrated this horror, as well. We must trace this illegal and horrendous agenda all the way back to the source, for our investigations and results to be effective, and for proper criminal charges to be brought to bear.

We cannot “drop the dollar to pick up a nickel”. We must be thorough and uncompromising in our collected facts and evidence for real justice to be actualized.
We intend on just that.

Mon, August 10, 2009 - 2:13 PM

Recipe for Destruction

Published: October 17, 2005

AFTER a decade of painstaking research, federal and university scientists have reconstructed the 1918 influenza virus that killed 50 million people worldwide. Like the flu viruses now raising alarm bells in Asia, the 1918 virus was a bird flu that jumped directly to humans, the scientists reported. To shed light on how the virus evolved, the United States Department of Health and Human Services published the full genome of the 1918 influenza virus on the Internet in the GenBank database.

This is extremely foolish.
The genome is essentially the design of a weapon of mass destruction.
No responsible scientist would advocate publishing precise designs for an atomic bomb,
and in two ways revealing the sequence for the flu virus is even more dangerous.

First, it would be easier to create and release this highly destructive virus from the genetic data than it would be to build and detonate an atomic bomb given only its design, as you don't need rare raw materials like plutonium or enriched uranium. Synthesizing the virus from scratch would be difficult, but far from impossible. An easier approach would be to modify a conventional flu virus with the eight unique and now published genes of the 1918 killer virus.

Second, release of the virus would be far worse than an atomic bomb. Analyses have shown that the detonation of an atomic bomb in an American city could kill as many as one million people. Release of a highly communicable and deadly biological virus could kill tens of millions, with some estimates in the hundreds of millions.

A Science staff writer, Jocelyn Kaiser, said, "Both the authors and Science's editors acknowledge concerns that terrorists could, in theory, use the information to reconstruct the 1918 flu virus." And yet the journal required that the full genome sequence be made available on the GenBank database as a condition for publishing the paper.

Proponents of publishing this data point out that valuable insights have been gained from the virus's recreation. These insights could help scientists across the world detect and defend against future pandemics, including avian flu.

There are other approaches, however, to sharing the scientifically useful information. Specific insights - for example, that a key mutation noted in one gene may in part explain the virus's unusual virulence - could be published without disclosing the complete genetic recipe. The precise genome could potentially be shared with scientists with suitable security assurances.

We urgently need international agreements by scientific organizations to limit such publications and an international dialogue on the best approach to preventing recipes for weapons of mass destruction from falling into the wrong hands. Part of that discussion should concern the appropriate role of governments, scientists and their scientific societies, and industry.

We also need a new Manhattan Project to develop specific defenses against new biological viral threats, natural or human made. There are promising new technologies, like RNA interference, that could be harnessed. We need to put more stones on the defensive side of the scale.

We realize that calling for this genome to be "un-published" is a bit like trying to gather the horses back into the barn. Perhaps we will be lucky this time, and we will indeed succeed in developing defenses for these killer flu viruses before they are needed. We should, however, treat the genetic sequences of pathological biological viruses with no less care than designs for nuclear weapons.

Ray Kurzweil, an inventor, is the author of "The Singularity is Near: When Humans Transcend Biology." Bill Joy, founder and former chief scientist of Sun Microsystems, is a partner at a venture-capital firm.
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Satyagraha October 31, 2009, 01:36:28 AM
UNITED STATES: Military resurrects deadly flu virus
22 October 2003

AUSTIN — The US military is attempting to resurrect the influenza virus that killed up to 40 million people in 1918. Several genes of the extraordinarily lethal “Spanish flu” have been isolated and introduced into contemporary flu strains. The new strain has proved to be lethal for mice, while the contemporary flu it was made from had hardly any effect.

The Spanish flu was highly infectious and killed a very high percentage of those infected, including many younger people. It caused life expectancy in the US in 1918 to drop by 10 years.

Despite the very dangerous nature of the 1918 virus, efforts to reconstruct it began in the mid-1990s, when Dr Jeffrey Taubenberger from the US Armed Forces Institute of Pathology succeeded in recovering and sequencing fragments of the viral RNA from preserved tissues of 1918 victims.

After partially unravelling the genetic sequence of the virus,
the scientists went a step further and succeeded
in creating a live virus containing two 1918 genes that
proved to be very lethal in animal experiments.

A resuscitation of the Spanish flu is neither necessary nor warranted from a public health point of view. Allegedly, the recent experiments sought to test the efficacy of existing antiviral drugs on the 1918 construct.

But there is would be no need for antiviral drugs against the 1918 strain
if it was not recreated in the first place.

“It simply does not make any scientific sense to create a new threat just to develop new countermeasures against it”, said Jan van Aken, a biologist with the anti-biological weapon group, the Sunshine Project.

“This particularly dangerous eradicated strain
could wreak havoc if released, deliberately or accidentally.”

Construction of new maximum security (BSL-4) laboratories for “bio-defence” research has been justified by Washington in part by citing the potential of the Spanish flu as a biological weapon. Influenza usually requires a low level of containment; but when scientists begin recombining virulence-related genes, the danger dramatically increases. The University of Texas Medical Branch's BSL-4 plans influenza “gene reassortment” experiments in maximum containment.

“This kind of research is creating a vicious circle and could prompt a race by bio-defence scientists to genetically engineer unthinkable diseases”, said Edward Hammond from the Sunshine Project.

“If Taubenberger worked in a Chinese, Russian or Iranian laboratory, his work might well be seen as the `smoking gun' of an offensive bio-warfare program”, noted van Aken.

A Sunshine Project briefing paper on the “Reconstruction of the Spanish Influenza Virus” is posted at <>.

From Green Left Weekly, October 22, 2003.
Visit the Green Left Weekly home page.

From: International News, Green Left Weekly issue #558 22 October 2003.
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: trailhound October 31, 2009, 01:36:39 AM

Lethal secrets of 1918 flu virus
Flu virus
Millions were killed by the virus
Scientists who recreated "Spanish flu" - the 1918 virus which killed up to 50m people - have witnessed its remarkable killing power first hand.

The lungs of infected monkeys were destroyed in just days as their immune systems went into overdrive after a Canadian laboratory rebuilt the virus.

The reason for the lethal nature of the 1918 flu was never fully understood.

But the experts behind this test say they have found a human gene which may help explain its unusual virulence.

This research provides an important piece in the puzzle of the 1918 virus
Darwyn Kobasa
Public Health Agency of Canada

They are hoping to help control any future pandemic and believe that the strain may hold clues that will help them.

Despite the large number of casualties at the time, doctors had no way to preserve tissue samples taken from infected patients, so researchers used an ingenious method to overcome this.

Frozen body

The preserved body of a flu victim buried in Arctic permafrost was exhumed, and they painstakingly extracted the genetic material needed to work out the structure of the H1N1 virus.

Then, in a maximum "biosafety" facility at Canada's National Microbiology Laboratory they reconstructed a fully functioning virus, and infected macaque monkeys to see what would happen.

Writing in the journal Nature, they reported that the results were startling. Symptoms appeared within 24 hours of exposure to the virus, and the subsequent destruction of lung tissue was so widespread that, had the monkeys not been killed a few days later, they would literally have drowned in their own blood.

The results match those seen when mice were infected in an earlier study and are very similar to those described in human patients at the time the virus was at its height.

Dangerous virus

Darwyn Kobasa, a research scientist with the Public Health Agency of Canada, and lead author of the research, defended the decision to recreate one of the most dangerous viruses in history.

He said: "This research provides an important piece in the puzzle of the 1918 virus, helping us to better understand influenza viruses and their potential to cause pandemics."

However, it is not the virus that is directly causing the damage to the lungs - it is the body's own response to infection.

Immune system proteins that can damage infected tissue were found at much higher levels following H1N1 infection compared with other viral infections.

Analysis at the University of Wisconsin at Madison (UW) revealed that a key component of the immune system, a gene called RIG-1 appeared to be involved.

Levels of the protein produced by the gene were lower in tissue infected with the 1918 virus, suggesting it had a method of switching it off, causing immune defences to run wild.

Many influenza virologists remain nervous about creating and experimenting with a reconstructed 1918 Spanish flu virus
Dr Jim Robertson
National Institute of Biological Standards and Control

This ability to alter the body's immune response is shared with the most recent candidate for mutation into a pandemic strain, the H5N1 avian flu.

Experts are worried that if the virus changes so that it can infect humans easily, it could again be far more lethal than normal seasonal flu.

"What we see with the 1918 virus in infected monkeys is also what we see with H5N1 viruses," said Yoshihiro Kawaoka, who led the analysis at UW.

"Things may be happening at an early time point (in infection), but we may be able to step in and stop that reaction."

Preparing for pandemic

Dr Ronald Cutler, an infectious diseases researcher at the University of East London, said: "Knowing how that over stimulation takes place could lead to the development of new methods to treat these diseases so we are better prepared for any future pandemic."

Dr Jim Robertson from the UK's National Institute for Biological Standards and Control, said the decision to recreate the virus was justified.

"Many influenza virologists remain nervous about creating and experimenting with a reconstructed 1918 Spanish flu virus, an extremely dangerous virus which disappeared from the world long ago.

"However, it cannot be denied that the information that has been derived from this experiment is exciting and represents an important milestone in understanding the severity of these highly pathogenic types of influenza viruses."

: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Satyagraha October 31, 2009, 01:39:14 AM

"The Search for the 1918 Spanish Influenza Virus"

      The 'Spanish' influenza pandemic killed approximately 40 million people in 1918-19, making it the worst infectious disease outbreak in history. However, the virus responsible was not isolated.

Understanding the origins of the 1918 virus, and the basis for its exceptional virulence, may have utility in the prediction of future influenza pandemics. Using modern molecular biology techniques, characterization of the 1918 virus can now be performed. RNA from the 1918 flu virus was isolated from formalin-fixed, paraffin-embedded lung tissue samples of victims of the 1918 influenza that had been stored in the archives of the Armed Forces Institute of Pathology (Washington, DC), and from frozen lung tissue of a victim buried in permafrost in Alaska. The sequences are consistent with a novel H1N1 influenza A virus. 

Analyses suggest that the 1918 virus belongs to the subgroup of influenza strains that infect humans and swine, not the avian subgroup. Recently we reported the complete sequence of the hemagglutinin gene of the 1918 virus. The sequences from the three cases show very little variation. Phylogenetic analyses suggest that the 1918 virus hemagglutinin gene, although more closely related to avian strains than any other mammalian H1 sequence, is mammalian, and may have already been adapting in humans before 1918.

: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Satyagraha October 31, 2009, 01:42:12 AM
J Virol. 2005 Sep;79(17):11533-6.
A single amino acid substitution in 1918 influenza virus hemagglutinin changes receptor binding specificity.
Glaser L, Stevens J, Zamarin D, Wilson IA, García-Sastre A, Tumpey TM, Basler CF, Taubenberger JK, Palese P.

Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029, USA.

The receptor binding specificity of influenza viruses may be important for host restriction of human and avian viruses. Here, we show that the hemagglutinin (HA) of the virus that caused the 1918 influenza pandemic has strain-specific differences in its receptor binding specificity. The A/South Carolina/1/18 HA preferentially binds the alpha2,6 sialic acid (human) cellular receptor, whereas the A/New York/1/18 HA, which differs by only one amino acid, binds both the alpha2,6 and the alpha2,3 sialic acid (avian) cellular receptors. Compared to the conserved consensus sequence in the receptor binding site of avian HAs, only a single amino acid at position 190 was changed in the A/New York/1/18 HA.

Mutation of this single amino acid back to the avian consensus
resulted in a preference for the avian receptor.

PMID: 16103207 [PubMed - indexed for MEDLINE]

: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Anti_Illuminati October 31, 2009, 02:12:21 AM

Deadly 1918 flu reborn for study

Cox News Service
AJC, October 6, 2005

ATLANTA — Federal and private researchers, including scientists at the Centers for Disease Control and Prevention, have re-created the influenza virus that killed 50 million people in 1918 — in hopes of helping the world prepare for a long-expected next pandemic of flu.

The work, hailed as a stunning scientific achievement, confirms what some scientists have long suspected: The lost 1918 virus was a bird flu that jumped species to attack humans, much like the avian flu strain that has killed at least 60 people in Asia since late 2003. It was conducted in three cities and completed in a high-security Atlanta laboratory.

The analysis reveals that the current avian flu strain, known as H5N1, has begun to acquire some of the mutations that apparently made the 1918 virus so lethal — though the researchers cannot say how long it might take for the current strain to accumulate them all.

The resurrection of the 1918 flu, which began with a sprinkle of molecules and ended with a living virus, is not without controversy. It is being questioned both for its inherent risks and for how useful its findings ultimately will be in devising antiviral drugs and vaccines.

The results, released Wednesday in simultaneous publications by the journals Nature and Science, "provide critical clues to the genesis of the 1918 pandemic and why it was so lethal," Drs. Julie Gerberding and Anthony Fauci, the directors of the CDC and the National Institute of Allergy and Infectious Diseases, said in a joint statement. "The findings reveal essential information to help us speed our preparation for — and potentially thwart — the next influenza pandemic."

In the Nature paper, Dr. Jeffery Taubenberger and colleagues from the Armed Forces Institute of Pathology in Washington reveal the complete genome of the 1918 virus, which they retrieved from tissues taken from flu victims: two young soldiers whose autopsy records were stored at their own institution, and a woman whose corpse was disinterred from Alaskan permafrost by a pathologist sympathetic to their efforts.

The group, who were originally outsiders to the tight-knit fraternity of flu virology, rocked the scientific world with a 1997 paper asserting that the long-lost 1918 virus — which vanished decades before the development of techniques that could have described it — could be retrieved.

Wednesday's paper made good on that boast. The group found that the virus was almost completely a bird-flu virus — not, as some had thought, a mixture of segments from both avian and human flus — and possessed a handful of mutations in each of its eight genes that probably occurred as the virus began to infect humans.

And in a second analysis, they compared the 1918 sequence with the genetic sequence of the avian flu now circulating in Asia, finding that the current bird flu shares some of those same mutations.

"In a sense, [the current bird flu] might be going down a similar path to what ultimately led to 1918," Taubenberger said. He suggested that with further research, virologists could provide an early-warning checklist of changes signalling what scientists fear most: bird flu's shift from a hard-to-acquire infection in people to one easily transmitted.

Mutation timeline unclear

It is not possible to say when those changes might emerge, he added. Scientists know the rate at which flu strains collect mutations as they circulate among humans, but they do not know how rapidly flu strains change when they move from one species to another as bird flu has done.

Since late 2003, bird flu has killed or caused the preventive slaughter of more than 100 million domestic fowl and wild birds in Asia. Almost all of the 116 people known to have been sickened by the virus are believed to have been infected by birds. The virus may have passed from person to person in a few cases but not in a sustained way.

The Taubenberger group's genome results were used to create the more controversial piece of research revealed Wednesday: the re-creation of a live virus containing almost all of the genetic components of the 1918 strain.

In a three-cornered collaboration using a process called "reverse genetics," a research group at Mount Sinai School of Medicine in New York used Taubenberger's sequence to re-create individual genes from the 1918 virus, and then passed them to Dr. Terrence Tumpey, a senior microbiologist at the CDC.

Tumpey and his colleagues worked under lab conditions designated "biosafety level 3+," a half-step below those used for the most dangerous organisms known, with additional precautions that are normally applied only to bioterror organisms. They inserted the genes in lab culture cells, where the components self-assembled into a living, reproducing virus.

The group then used the recovered virus in experiments on mice, chicken eggs and cultures of human lung tissue. It killed all the mice within days, as well as chicken embryos normally used to produce quantities of virus for vaccines. And it reproduced rapidly in lung cells, even in cell cultures made to mimic certain body tissues where flu cannot normally grow.

But analysis of the recovered virus did not reveal any single mutation that makes the 1918 flu virus, famous for killing young, healthy victims in days and sometimes in hours, so lethal.

"There is not a smoking gun," said Dr. John Treanor, of the University of Rochester School of Medicine, who studies pandemic vaccine development but was not involved in the research. "What we're seeing is that all the individual genes contribute, but there is no single gene in there that is sufficient to make that virus a killer."

The experiments pinpointed molecular terrain that drugs could be designed to attack, Tumpey said, adding: "I have already gotten messages from other scientists saying, 'I have an idea for targeting this.' "

Scientists hail findings

Scientists with no connection to the flu research hailed its results as a significant achievement in illuminating the historical record, but were divided on its usefulness for future pandemics.

"The studies do not add to ? what we need to do to develop a pandemic vaccine," said Dr. David Fedson, a longtime pharmaceutical researcher who now lives in France. The tasks ahead, formulating a vaccine, getting it licensed and distributing it as widely as possible, are not primarily scientific ones, he said.

Other scientists had mixed views on whether the research should have been undertaken at all. The Federation of American Scientists, which earlier this week criticized the CDC for withholding unrelated flu research data, supported the work, noting the CDC submitted the proposal to several research review committees, as well as the independent National Science Advisory Board for Biosecurity.

The CDC deserves praise for ascertaining in advance that currently available antiviral drugs would have protected researchers from becoming infected and spreading the virus, and also for inviting outside researchers to work at its Atlanta labs rather than distributing the re-created virus, said Dr. Michael Stebbins, the federation's director of biology policy.

But the nonprofit Sunshine Project, which opposes biological weapons research, disagreed. "We see no compelling scientific reason to re-create the virulent virus," said Edward Hammond, the project's director.
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Satyagraha October 31, 2009, 02:27:56 AM
Evidence of the ACTUAL ORIGINS of the 2009 “Pandemic Influenza”
 with a Glimpse into its Esoteric Symbolism

By A. True Ott, PhD, ND
August 1, 2009  (All rights reserved.)

In March of 2009, the World Health Organization (WHO) and the Center for Disease Control (CDC) announced an outbreak of “Swine Flu” in Mexico and in Southern California.  Within a few months, the “outbreak” increased in scope resulting in the WHO issuing a “Level 6 – PANDEMIC” alert. 

Both the WHO and the CDC announced in April, that the influenza virus responsible for the “pandemic” is a “novel triple reassortant virus” that combines H1N1 (swine) virus with H5N1 (avian) virus and Human flu virus, (H3N2).  Press releases ( sent to the major media outlets of the United States, Canada, and the U.K. further declared that such a “triple virus” had never been seen before, that it was “Novel” (i.e. completely new.)

This information is patently and absolutely FALSE
.  According to the CDC’s own magazine, “Emerging Infectious Diseases”, outbreaks of a “novel reassortant triple virus” have been occurring since 2005.  These outbreaks were just as significant as the California and Mexican cases, but for some reason, it was not reported in the mainstream media.
In the September, 2008 edition of the CDC’s own EID Journal, the story of the 2005 diagnosis and patient history of the same Swine/Bird/Human virus now identified as the “2009 Novel Swine Flu” is well documented.

Three short weeks after receiving a standard flu shot, a 17 year old boy in Wisconsin comes down with influenza symptoms.  Cultures taken from the boy, however, show that he is not suffering from a normal flu virus, but rather has a “novel triple virus” consisting of Avian, Swine and Human viruses.
The authors of the CDC’s published report are quick to not place any blame on the vaccine being the cause of the disease, but instead declare that the illness was most likely due to the boy assisting in the butchering of a number of pigs three days earlier.  However, further sampling of the area swine herds did not result in obtaining any “novel” flu viruses, and the boy only, and no other individual doing the swine butchering was infected. 

Moreover, the question of exactly how the boy obtained the H5N1bird virus is still unexplained nor even asked within the article.  (Even though the boy was in close proximity with a live chicken that was eventually “sacrificed in a religious (Jewish) ritual” in the home) – this fact was ruled out as a possible source of the bird-flu strain. This was likely due to the fact that the “bird-flu” strain originated in turkeys and not in chickens.
Human Case of Swine Influenza A (H1N1) Triple Reassortant Virus Infection, Wisconsin (
Triple reassortant H3N2 influenza A viruses, Canada, 2005. (

Upon closer inspection of the story, (i.e. following the footnotes) some very interesting facts become known.
1.  The “novel” strain of swine/avian/human flu was completely absent from any sampling of swine and humans from 1930 to 1998. Then, out of nowhere, the “reassortant” triple virus appears in North American swine herds in 1998.  What could have caused this to happen so suddenly?
The emergence of novel swine influenza viruses in North America. (

2.  Researchers discovered that the “reassortant” strains infecting the pigs were entirely HUMAN in origin, meaning they didn’t mutate naturally in the swine populations, but were introduced into the pigs by human intervention.
Genetic characterization of H3N2 influenza viruses isolated from pigs in North America, 1977-1999: evidence for wholly human and reassortant virus genotypes. (

This researcher concludes that the new virus was introduced by humans INTO the pig herds, not vice versa.

It is common practice that modern CAFO swine farms have strict sanitation standards designed not to provide protection to the humans entering the facility from catching disease from the pigs, but rather, to prevent the pigs from becoming infected by outside humans.  Moreover, these massive, corporate CAFOs (confined animal feeding operations) are constantly injecting the pigs with vaccines and steroid drugs to elicit rapid weight gains and growth.  After all, in the CAFO industry, time is big money – and the pigs must get to optimum market weight as quickly as possible.  These vaccines could easily explain how bird viruses mixed with human viruses ended up in the blood of swine herds in North America instantaneously.  Moreover, virus DNA is more apt to mutate or “drift” when exposed to steroids or growth hormones such as those routinely injected into large corporate farm swine herds.

So, where could the 17 year old Wisconsin boy have possibly contracted the current “novel” virus back in 2005? 

It is highly likely that the boy received a flu vaccine from
California-based vaccine giant, CHIRON’S 2004:HOT” LOT which had been

This would help explain the involvement of the New York health department, and why Novartis moved so quickly to purchase Chiron completely in 2005. 

Why has the CDC and the WHO apparently ignored these vitally important pieces of information, and why have they withheld it from the American public?  Why was the New York health inspector (Alexandra P. Newman) sent to Wisconsin by the CDC to investigate this case and author the paper, and why did it take three years (2005-2008) to complete it?


In a recent April 30, 2009 “update” the World Health Organization’s “INFOSAN” in conjunction with the United Nations’ “Food and Agriculture Organization" made some very interesting declarations, in light of the documentations outlined in this paper. 

On page 2 of the report, the experts correctly declare that “swine influenza viruses do not normally infect humans”.  The report further explains that in order for a human to become infected with a “swine virus” (i.e. in an “abnormal” situation) – the human would have to literally exchange bodily fluids with an infected pig.  However, it is also true that pigs can readily catch human flu viruses that are merely airborne, (thus the need to protect the CAFO pigs from human-borne infections.)

Furthermore, this April 30 report declares this sobering truth:

“The implicated (novel pandemic virus causing such world PAN-ic)

The obvious question then is simply, if it has never been found naturally in pigs, (as the Wisconsin study of 2005 amply corroborates) then WHERE DID IT COME FROM?  Why is it still being called “swine” flu, if has been shown to have never been found in swine? 
To view the full report, go to:
I submit most mysteries in life are like a giant Sudoko puzzle – and can often be solved through the use of logic and elimination of information that doesn’t fit.  What information does fit into this particular puzzle, and how can the missing squares in the 9X9 matrix be filled?

It is a fact that Dr. Jeffrey Taubenberger began working in the mid-90’s on reverse engineering the deadly 1918 virus that killed untold millions of people. 

It is a fact that he assembled his “team” at the U.S. Army Institute of Pathology in 1996 and officially began work on the “project” in 1997. 

It is a fact that in 1997, Taubenberger published a paper in the journal “Science” identifying that the 1918 killer virus was a “triple reassortant novel” virus containing genetic segments of Human, Swine, and Avian origin.  Taubenberger completes his “project” in 2003, then begins working for the NIH in the area of Vaccine development. 

In 2005, a Wisconsin boy is diagnosed with the same triple virus now declared a pandemic by the WHO in 2009, SHORTLY AFTER RECEIVING A FLU SHOT. 

It is also a fact
that the world’s largest multi-national pharmaceutical corporation, Novartis, applied for a patent for a vaccine designed to address a “novel reverse-engineered triple reassortant pandemic virus” on November 4, 2005 – just a week before the Wisconsin boy receives his flu vaccine – and a month before the boy develops the first case of “triple” virus.  This patent is granted in February of 2009, then a very short month later, the same “triple-virus” is publicized world-wide as a terribly deadly Mexican outbreak.    Within days, Novartis receives billions of dollars in vaccine contracts from panicked nations. 

Fact: the “novel swine flu” has an extremely low mortality rate compared with “seasonal flu”.  ( 

 In fact, the CDC and the WHO have quit listing the cases and the fatalities, quite possibly because of this fact.  They may be concerned that people will begin to ask: “This doesn’t appear to be that deadly, why all the hysteria calling for a headlong rush to implement mass vaccination in our schools and in pregnant women?”  The same people would likely then ask in the next breath:  “Could it be possible that the vaccine can likely be many times more dangerous than the disease itself??” 

Fact: I have  shown that the CDC and the WHO have misled America as to the history and origins of the “Triple Virus”, so why should we believe their projections about the coming waves of death unless vaccines are pushed?

So, using Sudoku puzzle logic, what fits in the missing blanks? 

It should be obvious that this “virus” is not natural and is a product of “reverse engineering” in U.S. Army labs.  Given all of the other information, that is the only conclusion that fits. It completes the puzzle very nicely.


It is also readily apparent that Novartis, headquartered in Basel Switzerland has a very close and cozy relationship with the Club of Rome, who in turn founded the WHO,

which in turn founded the “International Food Safety Authorities Network” (INFOSAN)

which works in joint unity with the United Nation’s F.A.O. (Food and Agriculture Organization.) 

INFOSAN and the FAO have recently advocated installing unrealistic regulations on U.N. member-nation’s food supplies – regulations that would benefit only the large corporate farms while bankrupting small independent farms.   

Moreover, they are the architects of CODEX ALIMENTARIUS, which restrict the flow of natural and organic health supplements to the world.         

Take a close look at the Symbols ( of these three organizations.

Notice the “serpent” on the staff of the WHO symbol – with the U.N. logo in the background. 
The U.N. logo shows the earth divided into 33 segments – symbolizing the 33 levels of universal freemasonry. 
The INFOSAN logo shows the earth constricted by wide strips – as if the earth is under its complete bondage and control.  This is sinister enough, I would submit – but lets take a look next at the FAO logo.


 At first glance, this international logo looks benign and harmless enough, doesn’t it?  First glances can be deceiving, however. 

Look closer, and you will see two Latin words in the circular logo. These words are: “Fiat Panis”.   According to the founders of FAO, the English translation of this is: “Let there be Bread”.   Simple enough, but who (or what) is destined to “control” the bread, - i.e. the world’s food?  Let’s see the dictionary’s definition of these two words.

According to, the word Fiat is described:
FIAT:  –noun
1.   an authoritative decree, sanction, or order: a royal fiat.
2.   a formula containing the word fiat, by which a person in authority gives sanction.
3.   an arbitrary decree or pronouncement, esp. by a person or group of persons having absolute authority to enforce it: The king ruled by fiat.
1625–35; < L: let it be done, 3rd sing. pres. subj. of fierī to become

So, for instance, a “fiat” currency simply means money that is decreed to be valid only upon the authority of a specific government and that’s all.

Next let’s take a look at the work “Panis”.

PANIS: The Panis are a class of demons in the Rig-Veda.  Derived from PANI-, a term for "bargainer, miser," especially applied to one who is sparing of sacrificial oblations. The Panis appear in RV 10.108 as watchers over stolen cows.

In case you didn’t know, the Rig-Veda is the Hindu holy book as equivalent in importance to the Hindu faithful as the Koran is to Islam, and the “Babylonian Talmud” is to the Jews.  As a matter of fact, many historians agree that, like the Talmud, the Rig-Veda had its origins in ancient Babylon – the land of modern-day Iraq.   The Grand-Dragon of Freemasonry himself, Albert Pike declared this to be the case in his seminal book:  “Indo-Aryan Deities and Worship as Contained in the Rig-Veda”.  Read excerpts from Pike’s book at:

It would appear, then, that the Logo “Fiat Panis” has much more to do with a hidden, esoteric and deeply occultic agenda than it does with supplying bread to a hungry world.

I would submit that it literally means: An authoritarian decree by powerful, hidden demonic entities hell-bent on stealing and controlling the world’s food supply.

But then, who believes in Demons in this crazy world??  Do the world’s elite meet in secrecy each year in a place called Bohemian Grove just to get drunk and party under the effigy of a gigantic Stone Owl? Is it just a bizarre co-incidence that GREAT HORNED OWLS just happen to be the conveyors of demonic wisdom according to the Rig-Veda??   
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: trailhound October 31, 2009, 02:36:52 AM
It would appear, then, that the Logo “Fiat Panis” has much more to do with a hidden, esoteric and deeply occultic agenda than it does with supplying bread to a hungry world.

I would submit that it literally means: An authoritarian decree by powerful, hidden demonic entities hell-bent on stealing and controlling the world’s food supply.

But then, who believes in Demons in this crazy world??  Do the world’s elite meet in secrecy each year in a place called Bohemian Grove just to get drunk and party under the effigy of a gigantic Stone Owl? Is it just a bizarre co-incidence that GREAT HORNED OWLS just happen to be the conveyors of demonic wisdom according to the Rig-Veda??   

: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: deconstructmyhouse October 31, 2009, 02:53:54 AM
14. the fao emblem (

The first version of an FAO emblem was in the form of a silver badge prepared by the Danish silversmith, Georg Jensen, for distribution to participants in the Second Session of the FAO Conference, held in Copenhagen from 2 to 13 September 1946. As may be seen from the illustration (above left), it showed a head of wheat, with the letters of FAO in approximately the same position as they appear on the emblem now being used, but with the name of the country — Denmark — where the motto now appears. According to Hambidge (1955), “Fiat panis” (Let there be bread) was selected as the FAO motto by the first Director-General, Sir John Boyd Orr. ( see info on Orr below)

Various designs were used for the emblem after 1946, but the general pattern has remained unchanged, and some of the earlier versions were still in use in 1980/81. One early design in gold on green still appears in these colours on the Organization's diplomatic pouches: it can be seen on the plaque at the Homestead Hotel which commemorates the holding of the Hot Springs Conference (see Figure 1). The version currently in widest use, however, is depicted above (right). It was designed by Mr. H. Engeler of what was then the Publications Service in April 1960, and was approved some time thereafter by Mr. B.R. Sen, then Director-General. The first published reference to its official approval and use appears to have been in Administrative Circular 77/31, dated 30 March 1977, which was directed toward achieving complete uniformity in the design used.

The emblem in its current version was registered on 1 July 1964 with the United International Bureaux for the Protection of Intellectual Property (BIRPI), the predecessor of the present World Intellectual Property Organization (WIPO), in accordance with the Paris Convention for the Protection of Industrial Property. Under this convention the emblems of international organizations are protected against use as trade marks, or as elements of trade marks, in countries that are members of the Paris Union.

The provisions of the above-mentioned Administrative Circular were updated in Administrative Circular 80/30, dated 21 March 1980, which provides that requests by parties outside FAO to use the emblem are to be dealt with by the Office of the Legal Counsel.

Apart from the facts that one Director-General selected “Fiat panis” as the motto, and that another Director-General approved the present design, it does not appear that any formal decisions were taken either to have an emblem or as to what it should portray. The emblem thus made its appearance on the FAO scene in an informal manner, and it came into use gradually, in an equally informal and somewhat irregular way. It began appearing in one of its earlier versions on some FAO documents in mid-1947. For example, it appeared on the cover of the Director-General's Second Annual Report to the Conference, dated July 1947, and on the cover of Unasylva, Volume 1, Number 1, dated July/August 1947. On the other hand, it did not appear on tile Report of the Third Session of the FAO Conference, issued in December 1947. Present practice is to show the full name of the Organization, or the emblem, on the covers of all the organization's printed material. Both often appear on the same cover.

sir john boyd orr:emblem designer, grandson of a Mason grand master:,_1st_Baron_Boyd-Orr (,_1st_Baron_Boyd-Orr)
John Boyd Orr was born at Kilmaurs, near Kilmarnock, East Ayrshire, Scotland, the middle child in a family of seven children. His father, Robert Clark Orr, was a quarry owner, and a man of deep religious convictions, being a member of a sect of the Free Church of Scotland. His mother, Annie Boyd, was the daughter of another quarry master, wealthier than Robert Orr, and grandmaster of a Freemason's Lodge.

The family home was well supplied with books, and his father was widely read in political, sociological and metaphysical subjects, as well as religion. As he grew older, John would regularly discuss these subjects with his father, brothers, and visiting friends.[1] There was also family worship each evening.

When John was five years old, the family suffered a setback when a ship owned by Robert Orr was lost at sea. They had to sell their home in Kilmaurs, and moved to West Kilbride, a village on the North Ayrshire coast. According to Kay, the new house and environment were a great improvement on Kilmaurs, despite the family's reduced means. The major part of his up-bringing took place in and around West Kilbride. He attended the village school until he was thirteen. Religion was then an important part of junior education in Scotland, and the school gave him a good knowledge of the Bible, which stayed with him for the rest of his life.[2]

At the age of thirteen, John won a bursary to Kilmarnock Academy, a significant achievement as such bursaries were then rare. The new school was some 20 miles (32 km) from his home in West Kilbride, but his father owned a quarry about two miles (3 km) from the Academy, and John was provided with accommodation nearby. His family cut short his education at the Academy because he was spending too much time in the company of the quarry workers (where he picked up a "wonderful vocabulary of swear words"), and he returned to the village school. There he became a pupil teacher at a salary of £10 for the first year, and £20 for the second. This was a particularly demanding time for the young Boyd Orr, as in addition to his teaching duties, and studying at home for his university and teacher-training qualifications, he also had to work every day in his father's business.[2]

After four years as a pupil teacher, at the age of 19 he won a Queen's Scholarship to study at a teacher training college in Glasgow, plus a bursary which paid for his lodgings there. At the same time he entered a three-year degree course in theology[3][4] at the University, for which the fees were also covered.
[edit] First encounters with poverty

As an undergraduate in Glasgow, he would explore the interior of the city, usually at weekends. He was shocked by what he found in the poverty-stricken slums and tenements, which then made up a large part of the city. Rickets was obvious among the children, malnutrition (in some cases, associated with drunkenness) was shown by many of the adults, and many of the aged were destitute. In his first teaching job after graduating M.A. in 1902, he was posted to a school in the slums. His first class was overcrowded, and the children ill-fed or actually hungry, inadequately clothed, visibly lousy and physically wretched. He resigned after a few days, realising that he could not teach children in such a condition, and that there was nothing he could do to relieve their misery.[5]

After working for a few months in his father's business, he taught for three years at Kyleshill School in Saltcoats, also a poor area, but less squalid than the slums of Glasgow.
[edit] Return to university

Boyd Orr needed to augment his teacher's salary, and decided to do so by instructing an evening class in book-keeping and accountancy. After intensive study he passed the necessary examinations, and duly instructed his class. The knowledge and skills he learned by studying for, and teaching, this class were to prove very useful in his later career.

However his heart was not in teaching, and after fulfilling his teaching obligations under the terms of his Queen's Scholarship, he returned to the University to study biology, a subject he had always been interested in since childhood. As a precaution, he entered simultaneously for a degree in medicine.

He found the university to be a very stimulating environment. Diarmid Noel Paton (son of the artist Joseph Noel Paton) was Regius Professor of Physiology, and Edward Provan Cathcart (E.P. Cathcart) head of Physiological Chemistry, both men of outstanding scientific ability. He was impressed by Samuel Gemmill, Professor of Clinical Medicine, a philosopher whose deep thinking on social affairs also influenced Boyd Orr's approach to such questions.[5]

Half-way through his medical studies, his savings ran out. Reluctant to ask his family for support, he bought a block of tenanted flats on mortgage, with the help of a bank overdraft, and used the rents to pay for the rest of his studies. On graduating, he sold the property for a small profit.

He graduated B.Sc. in 1910, and M.B. Ch.B. in 1912, at the age of 32, placing sixth in a year of 200 students. Two years later, in 1914, he graduated M.D. with honours, receiving the Bellahouston Gold Medal for the most distinguished thesis of the year.
[edit] Research career

On leaving the university, he took a position as a ship's surgeon on a ship trading between Scotland and West Africa, choosing this job because it offered the possibility of paying off his bank overdraft faster than any other. He resigned after four months, when he had repaid the debt. He then tried general practice, working as a locum in the practice of his family doctor in Saltcoats, and was offered a partnership there. Realising that a career in medicine was not for him, he instead accepted the offer of a two-year Carnegie research scholarship, to work in E.P. Cathcart's laboratory. The work he began there covered malnutrition, protein[6] and creatine[7][8] metabolism, the effect of water intake on nitrogenous metabolism in humans,[9][10] and the energy expenditure of military recruits in training.[11]
[edit] The beginnings of the Rowett Research Institute

On 1 April 1914, Boyd Orr took charge of a new research institute in Aberdeen, a project of a joint committee for research into animal nutrition of the North of Scotland College of Agriculture and Aberdeen University. He had been offered the post on the recommendation of E.P. Cathcart, who had originally been offered the job, but had turned it down in favour of a chair in physiology in London.

The joint committee had allocated a budget of £5,000 for capital expenditure and £1,500 for annual running costs. Boyd Orr recognised immediately that these sums were inadequate. Using his experience in his father's business of drawing up plans and estimating costs, he submitted a budget of £50,000 for capital expenditure and £5,000 for annual running costs. Meanwhile, with the £5,000 he had already been allocated he specified a building, not of wood as had been envisaged by the committee, but of granite and designed so that it could serve as a wing of his proposed £50,000 Institute. He accepted the lowest tender of £5,030, and told the contractors to begin work immediately. The committee were not pleased, but had to accept the fait accompli. When war broke out the contractors were told to finish the walls and roof, but to do no more for the time being.
[edit] War service

On the outbreak of the First World War he was given leave to join the British Army, and asked his former colleague Cathcart to help him obtain a medical commission in an infantry unit overseas. Cathcart thought he would be more useful at home, and his first commission was in a special civilian section of the R.A.M.C. dealing with sanitation. Several divisions of non-conscripted recruits were in training in emergency camps at home, some of them in very poor sanitary conditions. Boyd Orr was able to push through schemes for improvement in hygiene, preventing much sickness.[12]

After 18 months he was posted as Medical Officer to an infantry unit, the 1st Sherwood Foresters. He spent much of his time in shell holes, patching up the many wounded. His courage under fire and devotion to duty were recognised by the award of a Military Cross after the Battle of the Somme, and of the Distinguished Service Order after Passchendaele. He also made arrangements for the battalion's diet to be supplemented by vegetables collected from local deserted gardens and fields. As a result, unlike other units, he did not need to send any of the men in his medical charge to hospital. He also prevented his men getting trench foot by personally ensuring they were fitted with boots a size larger than usual.[12]

Worried that he was losing touch with medical and nutritional advances, he asked to be transferred to the navy, where he thought he would have more time available for reading and research. The army was reluctant to let him go, but agreed, since he was still a "civilian surgeon." He spent a busy three months in the naval hospital at Chatham, studying hard while practicing medicine in the wards, before being posted to HMS Furious. On board ship his medical duties were light, enabling him to do a great deal of reading. He was later recalled to work studying food requirements of the army.
[edit] Post-war expansion of the Rowett Research Institute

When Boyd Orr returned to Aberdeen in early 1919, his plan for a larger Institute had still not been accepted. Indeed, even his plans for the annual maintenance grant had to be approved by the Professor of Agriculture in Cambridge, T.B. Wood. Despite gaining the latter's support, his expansion plans were at first rebuffed, although he succeeded in having the annual grant increased to £4,000. In 1920 he was introduced to John Quiller Rowett, a businessman who seemed to have qualms of conscience[13] over the large profits he had made during the war. Shortly afterwards, the government agreed to finance half the cost of Boyd Orr's plan, provided he could raise the other half elsewhere. Rowett agreed to provide £10,000 for the first year, £10,000 for the second year, and gave an additional £2,000 for the purchase of a farm, provided that, "if any work done at the Institute on animal nutrition was found to have a bearing on human nutrition, the Institute would be allowed to follow up this work",[14] a condition the Treasury was willing to accept. By September 1922 the buildings were nearly completed, and the renamed Rowett Research Institute was opened shortly thereafter by Queen Mary.[15]

Boyd Orr proved to be an effective fund-raiser from both government and private sources,[16] expanding the experimental farm to around 1,000 acres (4.0 km2), building a well-endowed library, and expanding the buildings. He also built a centre for accommodating students and scientists attracted by the Institute's growing reputation, a reputation enhanced by Boyd Orr's many publications.[17] His research output suffered from the time and energy he had to devote to fund-raising, and in later life he said, "I still look with bitter resentment at having to spend half my time in the humiliating job of hunting for money for the Institute."[15]

Through the 1920s, his own research was devoted mainly to animal nutrition, his focus changed to human nutrition both as a researcher and an active lobbyist and propagandist for improving people's diets.
[edit] International and political work

Orr, by now Rector of the University of Glasgow, was elected as an independent Member of Parliament (MP) for the Combined Scottish Universities in a by-election in April 1945, and kept his seat at the general election shortly after. He resigned in 1946.

After the Second World War, Boyd Orr resigned from the Rowett Institute, and took several posts, most notably at the FAO, where his comprehensive plans for improving food production and its equitable distribution failed to get the support of Britain and the US. He then resigned from the FAO and became director of a number of companies and proved a canny investor in the stock market, making a considerable personal fortune. When he received the Nobel Peace Prize in 1949, he donated the entire financial award to organizations devoted to world peace and a united world government. (The American Friends Service Committee was one of his nominators.[18]) He was elevated to the peerage in 1949 as Baron Boyd-Orr.

In 1960 Boyd Orr was elected the first president of the World Academy of Art and Science, which was set up by eminent scientists of the day concerned about the potential misuse of scientific discoveries, most especially nuclear weapons.

The University of Glasgow has a building and the Boyd Orr Centre for Population and Ecosystem Health[19] named after him, and the University's Hunterian Museum holds his Nobel medal.
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Satyagraha October 31, 2009, 03:30:30 PM
Influenza Revisited

Jeffery K. Taubenberger* and David M. Morens†
*Armed Forces Institute of Pathology, Rockville, Maryland, USA; and †National Institutes of Health, Bethesda, Maryland, USA

This issue of Emerging Infectious Diseases includes a group of invited articles addressing pandemic influenza. Over the past 2 years, concerns about a new influenza pandemic caused by either an epizootic avian strain, such as H5N1, or by some other influenza virus have engaged top virologists, epidemiologists, and policymakers as well as the press and public (1,2). However, many scientific questions about the risk of a pandemic remain unanswered, and as science attempts to catch up on decades of relative neglect, fear and speculation have begun to mount. Such speculation has led to what the press has called "hysteria" in private stockpiling of antiviral drugs; this panic has even been compared to the widespread fear of an atomic bomb attack that gripped the United States in the late 1950s and early 1960s, when many citizens built and stocked underground fallout shelters.

In this climate, scientific and public health communities must continually update and review what is known about the risk of pandemic influenza and about options to prevent and control it. This group of articles is intended to serve as a modest database of current knowledge and informed opinion in several key areas, including the history of pandemic influenza and public health responses to it; influenza pathogenesis, natural history, and host immune responses to infection; and influenza prevention and treatment with drugs and vaccines.

Missing from the list of authors in this issue is a man whose insight, effort, and support probably did more to advance our understanding of influenza than the efforts of any other single individual over the past 30 years, John R. LaMontagne, whose untimely death in 2004 was a great loss to the scientific community (for additional information, see

John would have agreed with another visionary scientist, Hermann Pidoux (1808–1882), who observed that "epidemics are the lives of diseases." In an attempt to understand a disease as explosive and fatal as pandemic influenza, the classic emerging/reemerging infectious disease, its history has been self-consciously chronicled for several centuries. The importance of that effort was recognized during the pandemic of 1889 and strongly reinforced by the next pandemic in 1918–1919 (the so-called "Spanish flu," the deadliest pandemic in human history). We review the life cycle of pandemic influenza during the past century, including the pandemics of 1918, 1957, 1968, and 1977, as well as a feared nonpandemic in 1976, looking at pandemics from different angles, questioning whether they are predictable and, if they are, what telltale signs we should be looking for.

The answers to these questions may not be reassuring. The origin of the earliest human influenza virus yet identified, the 1918 pandemic virus, is still a mystery even after genetic sequencing and comparison with other historical and circulating influenza viruses (3,4). Though clearly descended from an avian virus, the 1918 strain is genetically unlike any other influenza virus examined over the past 88 years, which indicates that its immediate origin before the pandemic is an unknown source. Complicating problems of origin, all of the pandemic and epidemic influenza A viruses that have appeared since 1918 have been descendants of it, arising by either genetic drift, reassortment with prevalent avian viruses, or in 1 case (1977) by apparent release from a freezer.

Thus, little scientific basis exists for predicting whether the current enzootic/epizootic avian H5N1 virus will become pandemic: none of the known pandemic influenza events of the past 87 years seem to have much in common with the current H5N1 situation.

Another problem is learning about the mechanisms by which influenza A viruses, all of which are believed to be endemic in wild waterfowl, their natural hosts, acquire the capacities to switch hosts, produce diseases in these new hosts, and in some cases, establish the ability to propagate directly between them. While preliminary information about the first 2 of these capacities is gradually becoming known (5–7), little has been learned about the third. Thus, predicting whether current H5N1 viruses are moving in the direction of solving the ultimate challenge of host-switching/propagation in humans, or whether they are fundamentally incapable of doing so, is difficult.

Although science may yet offer little in the way of pandemic prediction, understanding the size of the influenza problem and the mechanisms by which influenza viruses cause severe and fatal disease, i.e., pathogenesis, is still important. Such knowledge is fundamental if we expect to prevent and control epidemics using public health measures and clinical therapies. Again, answers are elusive. Although influenza is a leading cause of death worldwide, measuring the total effect of deaths from influenza is impossible, in part because diagnostic records for a key risk group, the elderly, are incomplete and imprecise (8).

Influenza also kills by different mechanisms such as primary viral pneumonia, secondary bacterial pneumonia in virus-damaged lungs, and an acute respiratory distresslike syndrome possibly associated with overly brisk immune responses, as well as by cardiac and other pathways, and by exacerbating serious chronic diseases such as diabetes mellitus, renal diseases, and congestive heart failure. The problems of understanding influenza occurrence and pathogenesis are therefore complicated by the many different pathways that lead to severe disease and death and by the difficulty in determining the frequency with which these events occur.

Because of these uncertainties and knowledge gaps, establishing effective programs for public health control and personal protection is particularly important. Vaccines and drugs against circulating influenza viruses have been used for decades, but their efficacy in any future pandemic is difficult to predict because, with current knowledge, the causative agent of a future pandemic cannot be known in advance and may well be a novel virus whose susceptibility to existing drugs and vaccines has not been established. Important new technologies allow construction and pretesting of vaccines against all of the known influenza surface glycoproteins (16 hemagglutinins and 9 neuraminidases), although the likelihood that a new pandemic strain would be preventable by such vaccines cannot be known without an ability to predict its antigenic nature. Among additional strategies to overcome this limitation is development of "universal" vaccines based on antigens shared by many, and ideally all, influenza viruses.

The recent H5N1 epizootics in Southeast Asia serve as an important reminder of how few of the key determinants of pandemic influenza are really understood. If there is a single lesson to be learned from the articles in this issue, it is that, as expressed by contributor Anthony Fauci, more research is needed in many areas. We do not know whether pandemic influenza will outpace the increasingly vigorous research to contain it. But the race is on, the stakes are high, and the world is nervously watching.

Jeffery K. Taubenberger

Dr Taubenberger is chair of the Department of Molecular Pathology at the Armed Forces Institute of Pathology in Rockville, Maryland. His clinical interest is in diagnostic molecular genetic pathology. His research interests include the molecular pathophysiology and evolution of influenza viruses.

David M. Morens

Dr Morens is an epidemiologist with a long-standing interest in emerging infectious diseases, virology, tropical medicine, and medical history. He spent more than 6 years at the US Centers for Disease Control, followed by 17 years at the University of Hawaii. Since 1999, he has worked at the National Institute of Allergy and Infectious Diseases. He is an associate editor of Emerging Infectious Diseases.

   1. Fauci AS. Race against time. Nature. 2005;435:423–4.
   2. Webby RJ, Webster RG. Are we ready for pandemic influenza? Science. 2003;302:1519–22.
   3. Reid AH, Taubenberger JK, Fanning TG. Evidence of an absence: the genetic origins of the 1918 pandemic influenza virus. Nat Rev Microbiol. 2004;2:909–14.
   4. Taubenberger JK, Reid AH, Lourens RM, Wang R, Jin G, Fanning TG. Characterization of the 1918 influenza virus polymerase genes. Nature. 2005;437:889–93.
   5. Matrosovich MN, Matrosovich TY, Gray T, Roberts NA, Klenk HD. Human and avian influenza viruses target different cell types in cultures of human airway epithelium. Proc Natl Acad Sci U S A. 2004;101:4620–4.
   6. Shinya K, Hamm S, Hatta M, Ito H, Ito T, Kawaoka Y. PB2 amino acid at position 627 affects replicative efficiency, but not cell tropism, of Hong Kong H5N1 influenza A viruses in mice. Virology. 2004;320:258–66.
   7. Glaser L, Stevens J, Zamarin D, Wilson IA, Garcia-Sastre A, Tumpey TM, et al. A single amino acid substitution in 1918 influenza virus hemagglutinin changes receptor binding specificity. J Virol. 2005;79:11533–6.
   8. Thompson WW, Shay DK, Weintraub E, Brammer L, Cox N, Anderson LJ, et al. Mortality associated with influenza and respiratory syncytial virus in the United States. JAMA. 2003;289:179–86.

Suggested citation for this article:
Taubenberger JK, Morens DM. Influenza revisited. Emerg Infect Dis [serial on the Internet]. 2006 Jan [date cited]. Available from
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Anti_Illuminati October 31, 2009, 08:52:41 PM

Source (,F2400_P1001_ARCHIVE_NUMBER,F2400_P1001_USE_ARCHIVE:1001,20051006.2919,Y)

Numéro d’archivage    20051006.2919
Date publiée    06-OCT. -2005
Sujet    PRO> Influenza virus, 1918 pandemic strain: reconstruction (02)

A ProMED-mail post
ProMED-mail is a program of the
International Society for Infectious Diseases

Sponsored in part by Elsevier, publisher of Tuberculosis
Date:   Thu 6 Oct 2005
From:   ProMED-mail <>
Source:   Nature, 437, 794-795 (6 Oct 2005) / doi: 10.1038/437794a [edited]

[The following special report amplifies the information contained in the BBC News item posted yesterday and considers some of the issues and concerns raised by this singular achievement. The correct references for the 2 papers published simultaneously in Nature and Science are the following: Jeffery K.  Taubenberg et al. Nature 437, 889-893, 2005; and T. M. Tumpey et al. Science 310, 77 80; 2005. - Mod.CP]

The recreation of one of the deadliest diseases known could help us to prevent another pandemic. Or it might trigger one, say critics. It is thought to have killed 50 million people, and yet scientists have brought it back to life. In this issue of Nature, scientists publish an analysis of the full genome sequence of the 1918 human influenza virus. And in this week’s Science, researchers describe how they used that sequence to recreate the virus and study its effects in mice.

Some scientists have already hailed the work as giving unprecedented insight into the virus. Working out how it arose and why it was so deadly could help experts to spot the next pandemic strain and to design appropriate drugs and vaccines in time, they say. But others have raised concerns that the dangers of resurrecting the virus are just too great. One biosecurity expert told Nature that the risk that the recreated strain might escape is so high, it is almost a certainty. And the publication of the full genome sequence gives any rogue nation or bioterrorist group all the information they need to make their own version of the virus. Jeffery Taubenberger of the Armed Forces Institute of Pathology in Rockville, Maryland, is the lead author of the sequencing study. He says the work was necessary and the risks were low. The paper gives details of the final three genes; the sequences of the rest have already been published. [see: Characterization of the 1918 influenza virus polymerase  genes. Jeffery K. Taubenberg, Ann H. Reid, Raina M. Lourens, Ruixue Wang, Guozhong Jin & Thomas G Fanning. Nature 437, 889-893, 6 Oct 2005 <>].

The full sequence is strong evidence that the 1918 flu virus is derived wholly from an ancestor that originally infected birds. In contrast, the viruses that caused the flu pandemics of 1957 and 1968 arose when human and avian flu viruses infected the same person at the same time, allowing their genes to mix.

All 8 of the genome segments from the 1918 virus differ in important ways from other human flu sequences, suggesting that none of the genome came from a strain that had previously infected people. “It is the most bird-like of all mammalian flu viruses,” says Taubenberger. Pinpointing exactly which genetic mutations allowed the virus to jump to humans will enable scientists to recognize other bird viruses that could trigger a pandemic. Taubenberger’s team has already identified 25 changes in the protein sequences of the 1918 strain that have been present in subsequent human flu viruses. These mutations are likely to be particularly important, he says. One such change, in the polymerase gene PB2, was found in the virus isolated from the only human fatality in a 2003 outbreak of H7N7 bird flu in the Netherlands.

In the paper in Science (T. M. Tumpey et al. 310, 77 80; 2005), Terrence Tumpey at the Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, and his co-workers have used Taubenberger’s sequence to recreate the complete 1918 virus. When they used the strain to infect mice they found it was extremely virulent, and after 4 days had generated 39 000 times more virus particles in the animals’ lungs than a modern flu strain. “I didn’t expect it to be as lethal as it was,” says Tumpey. All the mice died within 6 days of infection with the 1918 virus and none with a contemporary virus.

The researchers compared the complete 1918 virus with strains in which some genes had been replaced by those of contemporary strains. They found that replacing the haemagglutinin gene, which helps the virus to enter cells, made it unable to kill mice. Replacing all 3 of the polymerase genes, which allow the virus to replicate, significantly reduced its virulence. The haemagglutinin gene is essential, says Tumpey. “But no single change or gene is the answer,” adds Taubenberger. “It’s a combination effect.” Future research will involve testing reconstructed viruses with and without certain mutations, to see which are the most important for virulence.

Information from this type of study will hopefully be of use in vaccine and drug design, but so far the work is more about obtaining a basic understanding of the virus than any immediate health benefits.

The studies have been praised as ground-breaking. “It’s a landmark,” says Eddie Holmes, a virologist at Pennsylvania State University in University Park. “Not only is this the 1st time this has been done for any ancient pathogen, but it deals with the agent of the most important disease pandemic in human history.” The team got permission to do the work from CDC head Julie Gerberding and Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, based in Bethesda, Maryland. But the studies have sparked fears among other researchers. “There most definitely is reason for concern,” says Richard Ebright, a bacteriologist at Rutgers University in Piscataway, New Jersey, who serves on biosecurity panels. “Tumpey et al. have constructed, and provided procedures for others to construct, a virus that represents perhaps the most effective bioweapons agent now known.”  

“This would be extremely dangerous should it escape, and there is a long history of things escaping,” says Barbara Hatch Rosenberg, a molecular biologist and member of the Federation of American Scientists’ Working Group on Biological Weapons. “What advantage is so much greater than that risk?”

Ebright agrees that there is a significant risk, “verging on inevitability”, of accidental release of the virus into the human population, or of theft by a “disgruntled, disturbed or extremist laboratory employee”. And there is the danger that a hostile nation might reconstruct its own version of the virus, he says, pointing out that any of these scenarios could result in a large number of deaths [including, however, many in the nation that released the virus. - Mod.JW]

Ebright also believes that using an enhanced biosafety level-3 lab for the work was inadequate. If the researchers were going to do the work at all, they should have used level 4, the strictest biosafety condition, he says. This requires experimenters to wear full body suits. In 2003, he points out, a SARS virus escaped accidentally from a level-3 lab in Singapore, and in 2004, 2 further escapes occurred from such labs in Beijing. Tumpey counters that enhanced level 3, which requires upper body suits and respirators, is safe enough. Disgruntled employees aren’t a concern either, he says, because he is the only one who works with the virus. The few researchers with access to the lab undergo extensive background checks, and retina and fingerprint scans are used to prevent any unauthorized entry to the lab. He adds that even if the virus did escape, it wouldn’t have the same consequences as the 1918 pandemic.  Most people now have some immunity to the 1918 virus because subsequent human flu viruses are in part derived from it. And, in mice, regular flu vaccines and drugs are at least partly effective against an infection with reconstructed viruses that contain some of the genes from 1918 flu.

The other potential threat comes from the availability of the full genome sequence, which has been put on the GenBank database—a condition of the paper’s publication. Anyone can order DNA to be made to a certain sequence, points out Jonathan Tucker, a policy analyst at the Center for Nonproliferation Studies in Washington DC. There are currently no governmental controls on what sequences can be used, says Tucker, although some DNA synthesis companies now screen their orders for pathogenic sequences. If someone wants to reconstruct the virus, says Taubenberger, “the technology is available”. Philip Campbell, editor-in-chief of Nature, says that although he did not seek advice on whether to publish the work, he has done so for previous flu-virulence and pathogen genome papers. He says that the benefits clearly outweigh the risks. Donald Kennedy, editor-in-chief of Science, agrees about the merits of publication. “I think we are going to depend on this kind of knowledge,” he says.

The US National Science Advisory Board for Biosecurity (NSABB) reached a similar conclusion about both studies, after calling an emergency meeting last week to consider the risks. But, concerned about public fears, it asked the authors of both papers to add a passage to the manuscripts stating that the work is important for public health and was conducted safely. Campbell says he is worried that government agencies will start seeking to be involved in the publishing process.
“We are happy to cooperate with the NSABB to consider the principles by which dual-use results can be published responsibly,” he says. “But government bureaucracies and committees may push to avoid perceived risks, at the potential expense of benefits to public security.”

Taubenberger admits that there can be no absolute guarantee of safety. “We are aware that all technological advances could be misused,” he says. “But what we are trying to understand is what happened in nature and how to prevent another pandemic. In this case, nature is the bioterrorist.”
[Byline: Andreas von Bubnoff]

: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Satyagraha October 31, 2009, 09:04:14 PM
Archive Number    20051005.2901
Published Date    05-OCT-2005
Subject    PRO/AH> Influenza virus, 1918 pandemic strain: reconstruction

A ProMED-mail post
ProMED-mail is a program of the
International Society for Infectious Diseases

Date: Wed 5 Oct 2005
From: ProMED-mail <>
Source: BBC News, Wed 5 Oct 2005 [edited]

1918 killer flu 'came from birds'

The Spanish flu virus that killed 50 million people in 1918-19 was probably a
strain that originated in birds, research has shown. US scientists have found
the 1918 virus shares genetic mutations with the bird flu virus now
circulating in Asia.

Writing in Nature -- see 
<> -- they say their
work underlines the threat the current strain poses to humans worldwide. A
second paper in Science reveals another US team has successfully recreated the
1918 virus in mice. The virus is contained at the US Centers for Disease
Control and Prevention [CDC] under stringent safety conditions. It is hoped to
carry out experiments to further understand the biological properties that
made the virus so virulent.

The virus was recreated from data produced by painstaking research by a team
from the US Armed Forces Institute of Pathology. Working on virus samples from
the remains of victims of the 1918 pandemic, the researchers were able to
piece together the entire genetic sequence of the virus.

They found the virus contained elements that were
new to humans of the time, making it highly virulent.

Analysis of the final 3 pieces of the virus' genetic code has
revealed mutations that have striking similarities to those found in flu
viruses found only in birds, such as the H5N1 strain currently found in south
east Asia.

Many experts believe it is only a matter of time before H5N1,
or a similar virus, causes many deaths in humans -- possibly after
combining [reassorting genome segments] with a human flu strain.

Crucially, the mutations identified by the US researchers were found
in genes which control the virus' ability to replicate in host cells.
The researchers say these mutations may have helped the 1918 virus
replicate more efficiently.

At this stage, they say the H5N1 strain shares only some, and not all, of
these mutations. But these mutations may be enough to increase the virulence
of the virus, and give it the potential to cause serious human infection
without first combining [reassorting genome segments] with a known human flu
The researchers believe the 2 other major flu pandemics of the 20th
century -- in 1957 and 1968 -- were caused by human flu viruses which acquired
2 or 3 key genes from bird flu virus strains. But they believe the 1918 strain
was probably entirely a bird flu virus that adapted to function in humans.

Julie Gerberding, director of the US Centers for Disease Control & Prevention (CDC), said:
"By unmasking the 1918 virus we are revealing some of the secrets that will help us predict and
prepare for the next pandemic."

Dr Jeffery Taubenberger, lead researcher of
the Nature study, said:
"Determining whether pandemic influenza virus strains
can emerge via different pathways will affect the scope and focus of
surveillance and prevention efforts."

Professor John Oxford, an expert in virology at Queen Mary College, London,
said the suggestion that the virus had the potential to jump between humans
without first combining [reassorting] with a human virus made it even more of
a threat. "This study gives us an extra warning that H5N1 needs to be taken
even more seriously than it has been up to now," he said.

Dr Terrence Tumpey, of the US CDC, defended the decision to recreate the 1918 flu virus.
He said:
"We felt we had to recreate the virus and run these experiments to
understand the biological properties that made the 1918 virus so exceptionally
deadly. "We wanted to identify the specific genes responsible for its
virulence, with the hope of designing antivirals or other interventions that
would work against virulent pandemic or epidemic influenza viruses."


: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Satyagraha October 31, 2009, 09:10:01 PM
Archive Number    20041007.2754
Published Date    07-OCT-2004
Subject    PRO> Influenza A virus, virulence, 1918 pandemic strain

A ProMED-mail post
ProMED-mail is a program of the
International Society for Infectious Diseases

Date: Thu 7 Oct 2004
From: ProMED-mail <>
Source: New York Times, Thu 7 Oct 2004 [edited]

Critical gene a suspect in lethal epidemic
By recreating the influenza virus that killed up to 50 million people in
1918-19, researchers may have identified the gene that turned it into one
of the most lethal in human history.

The gene, one of 8 in the virus, seems to have an unexpected capacity for
sending the body's immune system into overdrive, causing inflammation,
hemorrhage and death, the scientists report today in the journal Nature.

The research team, led by Dr Yoshihiro Kawaoka of the University of Wisconsin,
has been trying to determine just why the 1918 virus was so lethal and how
defenses could be devised if a similar virus appeared in the future.
Although the virus has long since perished, Dr Kawaoka and his colleagues
were able to recreate it because the composition of its genes had been
reconstructed from the preserved tissue of victims. The genes have been
reconstituted over the last few years by Dr. Jeffery K Taubenberger and
colleagues at the Armed Forces Institute of Pathology in Washington.

Drs Kawaoka, Taubenberger, and others have been reinserting
the 1918-type genes into ordinary influenza viruses to see whether they can
pinpoint which of the genes made the virus so lethal and how it did so.

In the latest of these experiments, which Dr Kawaoka reports today, a gene called
the haemagglutinin or HA gene seems to be largely responsible for the dire
effects of Spanish flu, as the 1918 epidemic is also known. Recreating such
a dangerous organism is not an experiment to be undertaken lightly. Dr
Kawaoka's approach required replacing the HA and another gene in a mild
influenza virus with the Spanish flu versions and infecting mice with the
novel agent. Because of the obvious hazards, he at first conducted the work
in the most secure type of biological laboratory, designated Biosafety
Level 4, one of which was available at the National Microbiological
Laboratory in Winnipeg, Canada. He said that after satisfying himself that
the souped-up virus was susceptible to an antiviral agent known as Tamiflu,
he transferred the research to a Biosafety Level 3 laboratory at the
University of Wisconsin.

Dr R Timothy Mulcahy, chairman of the university's biosecurity task force,
said that the chances of escape from the Biosafety Level 3 facility were
minimal and that Dr Kawaoka had been "extremely prudent" in starting out at
the higher level. "If there were an escape there would be treatments," Dr
Mulcahy said. He noted that another group of researchers had already worked
with similar engineered influenza viruses in a Level 3 facility owned by
the Department of Agriculture in Athens, Ga.

The HA gene studied by Dr Kawaoka's team is well-known to flu experts
because it changes from year to year. Since the protein made by the gene is
the one singled out for attack by the immune system, the body's defenses
are caught off guard each year as flu virus arrives with a novel version of
the protein to which the body has no prior immunity. The HA protein's role
is to latch onto the surface of human cells and then help the virus merge
into the cell's outer membrane. Researchers recently worked out the exact
3-dimensional structure of the Spanish flu version of the HA protein, but
could see no other function that it was designed to serve. The same is true
of the other Spanish flu genes recovered by Dr. Taubenberger. In the
current state of knowledge, the genes betray no clear hint of what made
[the virus] so lethal.

That makes it necessary to conduct experiments like Dr Kawaoka's, in which
researchers physically reconstruct the virus and try to understand how it
works. What he has now found is that the Spanish flu version of the HA
gene, in addition to its break-in and enter roles, seems able to trigger
the release of cytokines, the signaling agents with which the immune system
gears itself up for massive attack against an infectious agent.
Uncontrolled overdrive can make the immune system kill the body in order to
save it, through excessive inflammation. The virus carrying the Spanish flu
version of the HA gene produced high levels of cytokines in mice, Dr
Kawaoka says, and this is probably what led to the inflammation and lung
damage that killed them.

Dr Adolfo Garcia-Sastre, a flu expert at the Mount Sinai School of Medicine
who has constructed a similar virus, said the HA gene might be causing
extra virulence simply by helping the virus replicate better, not because
of any special effect on cytokine production.
But either way, the finding
helped focus attention on the gene's role, he said. Survivors of the 1918
epidemic have high levels of antibody to the engineered virus, Dr Kawaoka
reports, but people infected recently with a similar class of influenza
virus do not.

"Thus, a large section of the population would be susceptible to an
outbreak of a 1918-like influenza virus," he and his colleagues conclude.

[byline: Nicholas Wade]


: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Satyagraha October 31, 2009, 09:19:43 PM
Date: Tue, 23 Feb 1999 23:05:04 -0300
From: GPHIN 15 Feb 1999
Source: News reports, Mon 15 Feb 1999

Deadly 1918 virus resembled common swine flu,F2400_P1001_ARCHIVE_NUMBER,F2400_P1001_USE_ARCHIVE:1001,19990223.0245,Y

A frozen corpse and preserved samples from victims of the 1918 flu epidemic
that killed up to 40 million people worldwide show the virus resembled the
common swine flu, scientists reported Monday. 

Tissue samples from three people who died in the epidemic have provided
enough genetic material to allow researchers to sequence, or map, one key
gene of the virus, a team from the U.S. Armed Forces Institute of Pathology
wrote in the Proceedings of the National Academy of Sciences.  "The
existing strain to which the 1918 sequences are most closely related is
A/Sw/Iowa/30, the oldest classical swine flu strain,'' the scientific team,
led by Ann Reid and Jeffrey Taubenberger, wrote. 

Researchers have been eager to discover what made the 1918 strain of flu so
different -- and so deadly.  "The influenza pandemic of 1918 was
exceptionally severe, killing 20 to 40 million people worldwide, with
unusually high death rates among young, healthy adults,'' the team wrote. 

Scientists also wanted to know where the virus originated because that can
help doctors understand how best to fight the disease. But scientists
investigating the 1918 flu were stymied in part by the difficulty of
finding viable samples from people who have been dead for more than eight

Last year a team tried to get samples from people buried on the Norwegian
island of Spitzbergen, but they found the bodies were buried above the
permafrost and the tissues were not well enough preserved to provide good
genetic samples. 

The Armed Forces Institute of Pathology team used samples from the body of
an Alaskan Inuit who was buried in permafrost on the Seward Peninsula and
tissue preserved in formaldehyde from a 21-year-old soldier who died at
Fort Jackson, South Carolina, and a 30-year-old who died at Camp Upton, New

They managed to sequence the entire gene from the samples for
hemagglutinin, a protein the influenza virus uses to infect the cells
scientists look at first to determine a flu strain. 

Often, the virus passes from birds to pigs, where it takes on
characteristics that make it easier to pass to humans. The
Reid-Taubenberger team said it is not yet clear whether the 1918 virus came
to people straight from birds or passed through pigs first -- or whether it
passed from people to pigs. 

They noted that there had been an outbreak in the spring of a mild flu,
followed by an outbreak in the autumn among pigs and then the killer
epidemic in people. "This sequence of events supports the theory that the
1918 influenza spread from humans to swine,'' they concluded.

[Written by: Maggie Fox, Health and Science Correspondent]

: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Anti_Illuminati November 01, 2009, 01:17:57 PM
Risen from the dead: Can 1918 virus help defeat bird flu threat?
From Hospital Infection Control & Prevention | December 2005   

‘The road to hell is usually paved with good intentions’

In a high-containment laboratory along Clifton Road in Atlanta last summer, a mouse became the first living thing to inhale the 1918 pandemic influenza virus since it killed millions of people and vanished from the face of the earth. Predictably, it died.

After a decade of research that included digging up tissue from a flu victim buried in the Alaskan permafrost, the most infamous infectious disease agent in human history has been brought back to life.1,2 Its legendary virulence apparently came back with it. The research mice — which are not particularly fazed by human flu strains — died in three to five days. Unlike typical human flu, the infecting 1918 H1N1 strain replicated deep within the mice lungs, prompting an immune system hyperreaction — the so-called “cytokine storm” — which researchers suspect is a key to the virus’ virulence.

“There is something unique about the 1918 virus,” says Terrence Tumpey, PhD, the senior microbiologist at the Centers for Disease Control and Prevention who recreated the virus and “intranasally inoculated” the mice. “It is one of the [research] areas we really want to get into. Why does the virus target the deeper areas of the lung and kill mice so quickly?”

Ferrets actually are the preferred research animal in terms of mimicking human response to influenza, but the smaller mammals were chosen due to the extreme conditions required in the laboratory. Tumpey worked under enhanced biosafety level three conditions in a high-security lab at the CDC’s Clifton Road facility. The lab precautions were elaborate and redundant, including working with safety cabinets, isolation cabinets, gloves, gowns and wearing a powered air-purifying respirator body suit. He was required to change clothes and “shower out” of the lab, provide routine weekly written reports and notify agency officials immediately of any concerns related to biosafety or biosecurity.

Using “reverse genetics” — essentially reassembling genetic fragments into a whole, functioning microorganism — Tumpey and his fellow researchers built a virus that is to influenza what the Titanic is to ocean liners. When done, it contained the complete coding sequences of the eight viral gene segments from the 1918 pandemic strain. There below the electron microscope was the Spanish flu, so-called because of the popular misconception that it originated in Spain. For anyone who works in infectious diseases, this is akin to finding the Ark of the Covenant. The 1918 influenza pandemic still is retold like a ghost story, wherein a pathogen of unknown origin arises to sweep the earth and mysteriously disappears after killing as many as 50 million people worldwide, including an estimated 675,000 in the United States.

With warring nations under press censorship, Spain’s free press publicized the emerging 1918 pandemic and became forever branded as its country of origin. Ironically — considering that the virus now resides here again — the United States may have actually birthed the 1918 flu. Soldiers training at Fort Riley, KS, in March 1918 were among the first to fall ill and die. It was off to war for their comrades, many of whom may have been incubating the virus when they hit the trenches. Ultimately, the 1918 flu would kill nearly as many soldiers as their human enemies. Indeed, the 1918 influenza pandemic’s most striking feature was the unusually high death rate among healthy adults aged 15 to 34 years. Epidemiologists still look in puzzlement at the age/mortality charts, rising to a grim peak in the middle years when one should have maximum immunity to infectious diseases.

A soft-spoken, bespectacled 43-year-old, Tumpey paused for a second when asked what his first thoughts were when he realized he had successfully recreated the notorious 1918 influenza virus. In his answer he used the word “rescue,” a concept apparently not unusual to virologists, but a striking verb choice when one is bringing a natural-born killer back to molecular life.

“This represents an exciting time to be able to work with these viruses, to understand their molecular and biological properties and identify what additional targets could be looked at for the development of antivirals,” he replies. “Not only did I want to rescue the virus, but I also wanted to show that certain genes — certain viral proteins — associated with the 1918 virus were important for causing this virus to be so lethal. I thought of it from that standpoint. That we could see some clear benefits of rescuing this virus. We are [now] actually working on trying to prepare better vaccines against the 1918 virus that would give us information about vaccines against pandemic viruses.”

Ghoulish work

Tumpey was able to rebuild the virus because he had viral building blocks provided by Jeffery K. Taubenberger, MD, PhD — the Armed Forces Institute of Pathology researcher who spent 10 years reconstructing the 1918 pandemic flu strain bit by genetic bit. Two of the viral strains Taubenberger used came from autopsy remains of two U.S. soldiers who died in the great pandemic. The other genetic fragments required more ghoulish work in 1997, when investigators exhumed the frozen body of an Inuit woman who fell victim to the pandemic in a remote village on the Seward Peninsula of Alaska. As they hoped, viral fragments remained in the semipreserved body. Coincidentally, 1997 also marked the first appearance in Hong Kong of the bird flu strain causing much current anxiety: avian H5N1.

Looking at the reassembled 1918 virus, Taubenberger sees strong avian similarities, but it appears the deadly strain jumped into humans without going through the typical re-assortment with a circulating human flu strain. That is not particularly encouraging since it runs counter to the conventional wisdom that the H5N1 bird flu will not become transmissible in humans until it reassorts with a human flu strain. While the 1918 flu strain appears avian, it is unlike anything researchers have ever seen.

“Wherever it came from it came as a whole virus,” Taubenberger says. “This is true for all the segments of the virus. It looks kind of like a matched set. It suggests to us that it came from some animal that is a reservoir for influenza that we just don’t know about. It could be some other kind of wild bird, but it doesn’t look like your typical duck influenza viruses that people have been studying for the last 30 years. We don’t know where it came from, which is yet another tremendous mystery.”

The pig is the usual suspect, the classic “mixing vessel” for avian and human flu strains. Yet the genetic signature of the recreated virus suggests that pigs infected in 1918 actually may have acquired the virus from humans, he explains. Could another animal — one not typically associated with influenza mutation — have served as the intermediate host? The soldiers at Fort Riley, KS, were encamped with herds of horses and mules and all the manure that came with them. The manure was routinely burned to dispose of it, so plenty of opportunities for animal, human, and viral contact existed.

“Whether there was an intermediate host involved, like another mammal, unfortunately we just don’t know,” Taubenberger admits. “We think it is unlikely that the pig was the so-called mixing vessel or the intermediate host, but I can’t rule out some other animal — a horse? I can’t. I don’t know.”

The controversy surrounding his research is no mystery to Taubenberger. He is well aware of the accusations that it is irresponsible, but argues eloquently that finding the key to the virulence and transmissibility of the 1918 pandemic strain may help thwart the rise of H5N1 or future pandemic strains. “The key is to figure out how animal viruses adapt to humans and gain the ability to cause pandemics,” he says.

‘It is nature that is coming after us’

While extremely controversial, the achievement is staggering. One of the few precedents is the creation of a polio virus entirely from synthetic (e.g., nonliving) materials in 2002.1 That paper chillingly concludes, “Our results show that it is possible to synthesize an infectious agent by in vitro chemical-biochemical means solely by following instructions from a written sequence.” The lead researcher of the polio paper says the same thing could now be done for the 1918 H1N1 flu virus by following the recipe in the recently published papers.

“Yes, it can be done,” says Eckard Wimmer, PhD, professor in the department of molecular genetics and microbiology at the State University of New York in Stony Brook. “You could take this information in the public domain and recreate this virus. It would be difficult. Flu virus is much more complicated than polio virus. It would not be a piece of cake.”

Nevertheless, Wimmer argues that publication was the right strategy, noting that it will set off an explosion of research similar to the response when severe acute respiratory syndrome (SARS) suddenly appeared in 2002.

“This [SARS] corona virus came out of China,” he says. “When that virus first hit, nobody had an inkling what it was. It was fairly lethal. Depending on the age of the infected person it had a [mortality rate] of between 15% to 30%. There were no drugs, no vaccines. We really didn’t know how to grow this virus. People didn’t panic, but people could have panicked because it was really very scary.”

The World Health Organization quickly asked for global research on the emerging SARS virus, encouraging all clinical, molecular and virological research to be rapidly shared on the Internet. “Within a very short time — six or seven months — the virus was isolated, identified and sequenced,” Wimmer emphasizes. “Everything was put on the Internet and experiments for antiviral research and vaccines were initiated.”

Of course, like the 1918 virus, SARS disappeared, but the point is that the transparency with which it was met with was the absolute right scientific response, he emphasizes. “This [1918 research] will enormously stimulate research on influenza virus and open new avenues to protect us,” he says. “We are actually facing a threat, but not from bioterrorists who could synthesize this virus. It is nature that is coming after us. The bird flu that is coming out of Asia will eventually learn how to infect people. The enormous importance of this work on the 1918 flu is that it also was a bird flu virus. Research to develop new drugs against the influenza virus is of the utmost importance.”

Almost lost in the debate are the bioethical questions Wimmer faced when he used similar reverse genetic techniques to build a polio virus from scratch. Essentially a parasite, a virus replicates by invading a cell and using its existing biochemical materials to continue replication. Moreover, Wimmer “synthesized” the poliovirus genome, making an organism capable of replication and infection out of nonliving materials. Are such researchers creating life? A bioethicist who questions the wisdom of such research emphasizes that such research — even though viral in nature — is essentially cloning.

“There is a lot of discussion about human cloning and the ethics of it, but the science is very primitive,” says Arthur Caplan, PhD, director of the Center for Bioethics at the University of Pennsylvania in Philadelphia. “Engineering viruses, engineering microbes, reconstructing nasty pathogens — people are doing that. It is not hypothetical. People are getting very good at microbial genetics. I think it is only our vanity — thinking that we are important — that makes us forget that microbes can be more important. This is a very dangerous attitude to take.”

‘Unfortunately, it is an ideal weapon’

Others see danger of a more calculated variety, particularly since the 1918 viral genome was published and can now be recreated by other laboratorians using entirely synthetic materials. Among those questioning the wisdom of the research is Kenneth Alibek, MD, PhD, DSc, former chief scientist and deputy director of bioweapons research in the former Soviet Union.

Born Kanatjan Alibekov in the Soviet Republic of Kazakhstan, Alibek oversaw bioweapons research and development involving such pathogens as smallpox, anthrax, and viral hemorrhagic fevers. Now a U.S. citizen, he changed his name when he defected to the United States in 1992. Weaponizing influenza — particularly the 1918 strain — was discussed by Soviet researchers, says Alibek, now a distinguished professor in the department of molecular and microbiology at the National Center for Biodefense at George Mason University in Washington, DC.

“It was always under consideration,” he says. ”The Soviet Union was trying to start some things, but it never came to developing actual weapons because the viruses that were available at that time had very low virulence and a low morality rate. But when we talk about this type of virus [1918], of course there is a much a higher mortality rate. The probability that some other country will be interested in possible development of this as a biological weapon is very high. I don’t think that terrorists would be able to do something in terms of success with this virus, but for rogue states, it could be the case.”

It has been argued that influenza would not make a good bioweapon since it could not be controlled once released, and even if you developed a vaccine the weaponized virus still would be subject to ongoing mutation. Nevertheless, Alibek says the sheer virulence and transmissibility of the 1918 strain make it attractive as a bioweapon.

“This virus has a very high transmission rate — the highest rate known to man [for influenza],” he says. “Second, it can be grown easily using different techniques. The mortality rate for regular influenza virus is not so high, but for this virus the mortality rate was between 2% to 5%. Unfortunately, it is an ideal weapon.”

Given his unique background, Alibek is difficult to dismiss as an alarmist. Yet his warnings about the research were not heeded, he says. “My position was always absolutely obvious and clear,” he tells Hospital Infection Control. “It was a really bad idea. I had a discussion about this a couple of years ago with some of the scientists involved in the study of this virus. I said it is not a good idea, but if a decision was made to finish this work it shouldn’t be published.”

Prior to publication, the 1918 virus research was reviewed by the National Science Advisory Board for Biosecurity, an advisory committee to the U.S. government. Julie Gerberding, MD, MPH, director of the Centers for Disease Control and Prevention, and Anthony Fauci, MD, director of the National Institute for Allergy and Infectious Diseases, issued a joint statement that read in part: “The rationale for publishing the results and making them widely available to the scientific community is to encourage additional research at a time when we desperately need to engage the scientific community and accelerate our ability to prevent pandemic influenza. . . . Moving forward with research conducted by the world’s top scientists and openly disseminating their research results remain our best defense against H5N1 avian influenza virus and other dangerous pathogens that may emerge or re-emerge, naturally or deliberately.”

Alibek is skeptical that insights gained into the 1918 virus can be used to thwart the emerging bird flu threat. “It’s a different virus,” he says. “It is not H5N1. I am kind of doubtful how much information we will get from this Spanish flu virus. There would be a much higher probability [of success] just to start with all possible isolates of H5N1 virus, which are already available. That might produce real knowledge about how to fight this [avian] influenza, but not a virus that was infecting people a century ago.”

Advised that the CDC confirmed for this report that it already is working on a 1918 vaccine, Alibek could hardly contain the incredulity that rang through his thick Russian accent.

“First, we create the problem and then we use a huge amount of money to solve the problem,” he says. “If this work had not been done nobody would be developing a vaccine. It’s like, ‘Let’s create the disease and then we will try and fight it.’ It is absolutely insane. People can say they had good intentions and they will develop a new vaccine and so forth. Of course, their explanation is that they had good intentions, but I say the road to hell is usually paved with good intentions.”

‘It’s not Ebola’

Taubenberger, the man who has dedicated his career to restoring the virus and solving its mysteries, says the risks were weighed against the rewards.

“Certainly, we can not say there is no risk,” he says. “We thought about that at the very beginning when we decided to do this project. But the risk of that [bioterrorism] is pretty low compared with the benefits that could come out of studying the 1918 virus. Here was a naturally occurring virus that killed millions of people. Pandemics occur on a similar regular basis and we don’t understand how they work. It would very beneficial if we could understand the basic rules of how this happened, so that we could ultimately prevent it from happening [again]. We feel that the public health good from this project far, far outweighs the risk.”

Besides, the world has changed considerably since 1918, when there were no antibiotics, no influenza vaccines, no antivirals and viruses themselves were as yet undiscovered. The 1918 H1N1 flu strain would not find its human host as defenseless today. The virus is susceptible to the four currently available antiviral medications, which can minimize flu effects if taken shortly after infection. In addition, antibiotics could presumably stave off some portion of the bacterial coinfections that were responsible for so many of the 1918 deaths. Current vaccines appear to muster at least partial immunity to the strain, and humans may now even have some residual immunity through successive exposures to natural recurring flu and receipt of the annual seasonal vaccine.

“The ideal thing would be to develop a seed stock [vaccine] against 1918, but even the modern human virus vaccine would provide some protection,” Taubenberger says. “It’s not perfect, but there would be some protection. Certainly, 1918 was an incredibly lethal flu virus. The numbers of dead are astounding, but you also have to understand that basically everybody on earth breathed in this virus. The case fatality rate in the U.S. in 1918 — without vaccines, without antivirals, without antibiotics — was around 2%. That is terrible — the worst flu ever — but it’s not Ebola.”

The CDC is sufficiently concerned about the virus that it recently added it to its list of select agents and toxins. Acknowledging that it now is possible for those with knowledge of reverse genetics to reconstruct this virus, the CDC stated in making the announcement that it had been advised that the “molecular properties that enabled the 1918 pandemic influenza virus to cause such widespread illness and death are not completely understood and that it is not known how virulent the reconstructed virus would be in the population today.”

There currently are 41 other agents and toxins listed as select agents under the Public Health Security and Bioterrorism Preparedness and Response Act of 2002. As with the other agents, all scientists and researchers that possess, use or transfer the 1918 strain of influenza or the eight key gene regions of the 1918 virus are required to register with the CDC. The CDC also announced it will not distribute any of its 1918 viral isolates, but may allow other researchers to work with them at the CDC.

Created from ‘scratch’ in months

The U.S. restrictions are well and good, but do not address Alibek’s concern that researchers in another country could simply follow the published “recipe” and create the 1918 strain.

“If — as should be the case — transfer of the plasmids is restricted, then it would be necessary for someone attempting reconstruction to generate the plasmids again,” explains Richard H. Ebright, PhD, a professor of chemistry at Rutgers University in New Jersey. “The plasmids could be generated by de novo synthesis. There are a host of corporations that provide commercial gene and genome synthesis. To construct eight plasmids — each about 4,000 base pairs in size — would be a matter of a month or two months and moderate costs. They also could be constructed easily in major research labs. To go from ‘scratch’ to live fully infectious particles would be a matter of months.”

Beyond that there is always the possibility that well intended researchers may accidentally allow the virus to escape from the lab, he notes. Ebright, who is doubtful that sufficient residual immunity remains in the human population to provide much protection, points out there is no current direct vaccine match and antivirals are in extremely short supply. “I believe this research should not have been done,” he says. “The researchers have deliberately reconstructed a virus that has been extinct for more than eight decades, and when last present killed 1% of the world’s population.”

A scholar with a penchant for succinct analysis, Ebright lines his points up like dominos. “Overall, this poses three sets of risks,” he begins. “It poses a risk of accidental release, it poses a risk of deliberate release by a disturbed, disgruntled or extremist employee of a laboratory, and it poses the risk of clandestine reconstruction and deliberate release by a hostile party. In any one of those three scenarios, there would be the potential for significant loss of life and significant economic disruption.”

Echoing Alibek’s sense of irony, he adds, “It will be possible to build an effective vaccine, but the remarkable point here is to create a pathogen for the expressed purpose of developing a countermeasure. There is a logical lapse. The ethical barrier that would prohibit somebody from doing this has been breached by the fact that the work already has been performed and approved. It is a threat that must be considered. It would be prudent to produce and stockpile vaccine against this threat.”

Indeed, bioterrorism fears have prompted massive smallpox immunization campaigns among the military and health care workers in recent years, even though that virus has been completely eradicated in nature. Now, with restoration of the 1918 influenza virus we have another “demon in the freezer,” as the frozen stores of smallpox virus at the CDC and in Russia have been described. That raises the possibility of future mass immunizations against the 1918 flu, a pathogen that is so unusual that even its fully recreated genetic sequence doesn’t explain its origins. Is it possible that the 1918 strain was some kind of viral anomaly that was very unlikely to arise again in nature? “I guess that is certainly possible,” Taubenberger concedes.

Yet even if it had never recurred in nature, some other group of researchers may have eventually pieced the 1918 virus together. The Everest of the infectious disease world was not going to stay unclimbed for lack of trying.

“We knew all along that the [genetic] sequence would eventually be published, so we wanted to provide a clear public health benefit to rescuing this virus and understanding it.” Tumpey argues. “If it wasn’t done by Jeffery Taubenberger, there were others that were interested in it. Others had tissues and could do this work. We knew this day would come.”


   1. Taubenberger JK, Reid AH, Lourens RM, et al. Characterization of the 1918 polymerase genes. Nature 2005 Oct 6; 437(7,060):889-893.
   2. Tumpey TM, Basler CF, Aguilar PV, et al. Characterization of the reconstructed 1918 Spanish influenza pandemic virus. Science 2005; 310(5,745):77-80.
   3. Jeronimo C, Paul AV, Wimmer E. Chemical Synthesis of Poliovirus cDNA: Generation of Infectious Virus in the Absence of Natural Template. Science 2002; 1,018:1,016-1,018.
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Anti_Illuminati November 01, 2009, 05:38:37 PM
Blast from the past: 'Bird Flu': From PsyOP and population control to "WW4"
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Satyagraha November 06, 2009, 08:16:12 AM

September 10, 2008 16:45
In the Ukraine, began joint exercises with the United States to combat avian flu

International Ukrainian-American exercises in emergency response "Raf End Ready 2008" started today in Lviv. Their purpose is working out methods to combat avian influenza and the provision of international assistance in the event of an outbreak and a pandemic of the disease.

The exercise based Samborskii poultry engagements MOE, Ministry of Health, the Security Service of Ukraine, Ministry of Interior, Ministry of Foreign Affairs, Defense, Ministry of Transport, Ministry of Agrarian Policy, Ministry of Economy, Goskomvetmeditsiny, Customs Service, State Border Service. From the American side - the National Guard of California and California Disaster Medical Service, told Itar-Tass at the headquarters of Emergency in Lviv region.

In Ukraine, dangerous for human avian influenza virus Eych5-en1 was first recorded in wild birds in early October 2005 on the border with Romania in the Odessa region. In response to the outbreak Eych5-en1 in the Crimea in December of that year as a precaution were culled nearly 170 thousand heads of poultry.  

In mid-February 2006 the virus was found in Odessa Zoo in January 2008 in the poultry farm "Lobzenko" in the village of Falling in the Crimea. While no confirmed cases of avian influenza in Ukraine are not registered, however this does not exclude the possibility of epidemiologists. Among the sources of contamination of a deadly virus, experts say - the illegal importation of large quantities of animal products.

According to official data from the International Epizootic Bureau in 2007, highly pathogenic avian influenza was reported in 42 countries. Since early 2008, the disease has already been registered in Ukraine, Israel, Britain, China, Vietnam, Egypt, India, Iran, Turkey, Germany and Thailand.


Cooking up viruses.... what ingredients would you include to make sure:
John C. Kash,1* Christopher F. Basler,2 Adolfo García-Sastre,2 Victoria Carter,1 Rosalind Billharz,1 David E. Swayne,3 Ronald M. Przygodzki,4 Jeffery K. Taubenberger,4 Michael G. Katze,1,5 and Terrence M. Tumpey3

1. Its virulent and would spread among the population like wildfire (like 1918 Flu)

2. It's deadly (like Avian Flu)


Flashback: CDC to Mix Avian, Human Flu Viruses in Pandemic Study
Published on 04-28-2009
Source: CIDRAP News

Jan 14, 2004 – One of the worst fears of infectious disease experts is that the H5N1 avian influenza virus now circulating in parts of Asia will combine with a human-adapted flu virus to create a deadly new flu virus that could spread around the world.

That could happen, scientists predict,
if someone who is already infected with an ordinary flu virus
contracts the avian virus at the same time.

The avian virus has already caused at least 48 confirmed human illness cases in Asia, of which 35 have been fatal. The virus has shown little ability to spread from person to person, but the fear is that a hybrid could combine the killing power of the avian virus with the transmissibility of human flu viruses.

Now, rather than waiting to see if nature spawns such a hybrid,
US scientists are planning to try to breed one themselves—
in the name of preparedness.

The Centers for Disease Control and Prevention (CDC) will soon launch experiments designed to combine the H5N1 virus and human flu viruses and then see how the resulting hybrids affect animals. The goal is to assess the chances that such a "reassortant" virus will emerge and how dangerous it might be.

CDC officials confirmed the plans for the research as described recently in media reports, particularly in a Canadian Press (CP) story.

Two ways to make hybrids

The plans call for trying two methods to create hybrid viruses, CDC spokesman David Daigle told CIDRAP News via e-mail.
One is to infect cells in a laboratory tissue culture with H5N1 and human flu
viruses at the same time and then watch to see if they mix.

For the human virus, investigators will use A (H3N2), the strain that has caused most human flu cases in recent years, according to the CP report.

The other method is reverse genetics—assembling a new virus with sets of genes from the H5N1 and H3N2 viruses. Reverse genetics has already been used to create H5N1 candidate vaccines in several laboratories, according to Daigle. The National Institutes of Health (NIH) said recently it would soon launch a clinical trial of one of those vaccines.

Of the two methods, the co-infection approach was described as slower and more laborious, though closer to what happens in nature.

Any viable viruses that emerge from these processes will be seeded into animals that are considered good models for testing how flu viruses behave in humans, according to Daigle. The aim will be to observe whether the animals get sick and whether infected animals can infect others.

The World Health Organization (WHO) has been "pleading"
for laboratories to do this research, because it could provide some evidence
to back up the agency's warnings about the risk of a flu pandemic,
according to the CP report.

Klaus Stohr, head of the WHO's global influenza program, was quoted as saying that if none of the hybrids caused disease, the agency might be inclined to dial down its level of concern. But if the experiments produce highly transmissible and pathogenic viruses, the agency will be more worried, he said.

Safety precautions

Because of the obvious risks in creating viruses with the potential to spark a pandemic, the work will be done in a biosafety level 3 (BSL-3) laboratory at the CDC in Atlanta, Daigle told CIDRAP News.

"We recognize that there is concern by some over this type of work. This concern may be heightened by reports of recent lab exposures in other lab facilities," he said. "But CDC has an incredible record in lab safety and is taking very strict precautions."

Daigle said the US Department of Agriculture requires that highly pathogenic avian influenza (HPAI) viruses be treated as "Select Agents" and that research on them must be done in BSL-3 labs with "enhancements." These include "special provisions to protect both laboratory workers and the environment."

BSL-3 is the second highest level of laboratory biosecurity. It is used for work with pathogens that may cause serious or potentially lethal disease if inhaled, such as tuberculosis or St. Louis encephalitis, according to the CDC.

CDC experiments with HPAI viruses have to pass reviews by the agency's Institutional Biosafety Committee and Animal Care and Use Committee, Daigle said. The facilities involved are inspected by the USDA and the CDC's Office of Safety and Health, and staff members who work with Select Agents require special clearance.

It's been done before

The upcoming experiments will not break entirely new ground for the CDC, the CP story revealed.
The agency already has made hybrid viruses with H5N1
samples isolated from patients in Hong Kong in 1997
when the virus first caused human disease.

The results of that research have not yet been published, and the CDC has said little about them. In the CP report, Dr. Nancy Cox, head of the CDC's influenza branch, commented only, "Some gene combinations could be produced and others could not."

Daigle added little to that. He said, "The reassortment work with the 1997 isolate was intermittently interrupted with SARS [severe acute respiratory syndrome] and then the 2004 H5N1 outbreak. We are currently concentrating our efforts on understanding the pathogenicity of the 2004 strains (non-reassortants) in mammalian models."

He said the CDC hopes to prepare a report on that research "in the near future."

See also:

CDC information on biosafety levels
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Satyagraha November 06, 2009, 09:19:12 AM
So what are we finding in the Ukraine?

Referencing Moshe, who claimed Baxter was releasing a bioweapon in the form of a vaccine.
Baxter's lab is in the Ukraine.
Professor Moshe had called into a live radio show by Dr. A. True Ott, broadcast on Republic Broadcasting claiming to be a microbiologist who wanted to supply evidence to a States Attorney regarding tainted H1N1 Swine flu vaccines being produced by Baxter BioPharma Solutions. He said that Baxter’s Ukrainian lab was in fact producing a bioweapon disguised as a vaccine. He claimed that the vaccine contained an adjuvant (additive) designed to weaken the immune system, and replicated RNA from the virus responsible for the 1918 pandemic Spanish flu, causing global sickness and mass death.

Ukraine "mutated" H1N1 Swine Flu has killed 3000 people very quickly,

Symptoms: 8.4 Clinical, pneumonic plague

1. Primary pneumonic plague has an incubation period of 2 to 4 days.

2. The onset is acute and the course is fulminant with fever, chest discomfort, general malaise, hypotension and severe pneumonia, with a productive cough and bloody sputum.  This is usually associated with pleural effusion. (pleural effusion - increased amounts of fluid within the pleural cavity, usually due to inflammation.

Patients who cough are very contagious. At this point another person can be infected by direct person-to-person transmission.

It takes the form of a very rapidly progressive pneumonia with almost 100% mortality within a few days.

Secondary pneumonic plague initially takes the form of interstitial pneumonia with a small amount of thick, viscous sputum, subsequently progressing to the symptoms described above. It is striking how unremarkable the auscultatory findings are. It is possible, but not formally proven, that Yersinia pestis increases its virulence after repeated passage via the lungs.

Archive Number    20091105.3827
Published Date    05-NOV-2009
Subject    PRO/AH/EDR> Influenza pandemic (H1N1) 2009 (91): Ukraine


A ProMED-mail post
ProMED-mail is a program of the
International Society for Infectious Diseases

Date: Thu 5 Nov 2009
Source: Agence France-Presse report [edited]

86 people have died in Ukraine from flu and respiratory infections, the
health ministry said on Wednesday [4 Nov 2009], in an epidemic the World
Health Organization said could be largely due to the pandemic (H1N1) 2009
influenza virus.

The ministry said that almost half a million cases of flu
and acute respiratory infections had been recorded since mid-October 2009
in this country of 46 million, while 24 000 people have been hospitalised.
Some 148 000 cases have been recorded in the past 24 hours, it added.

The epidemic is concentrated in the west of the country, which borders 4
European Union states, but a growing number of cases are being reported in
the capital Kiev. "As the pandemic (H1N1) 2009 virus has rapidly become the
dominant influenza strain worldwide, it can be assumed that most cases of
influenza in Ukraine are caused by the pandemic (H1N1) 2009 virus,
" the WHO
said on Tuesday [3 Nov 2009].

FAIL: very few people are confirmed dead due to the H1N1 virus.

Lyudmila Mukharska, Ukraine's deputy chief health officer, said the
authorities had confirmed that 5 of the dead had died of the pandemic [?]
H1N1 virus
. She vehemently denied rumours that the west of the country was
suffering from an outbreak of plague, saying that it was "H1N1 that is
circulating in Ukraine."

WHO has sent a team of 9 experts to Ukraine to help the authorities with
the situation. The country is suffering from an above-average infection
rate. Prime minister Yulia Tymoshenko has personally overseen a delivery of
anti-flu medicines in the middle of the night, and pro-Western President
Viktor Yushchenko even called on NATO for help.

"Many questions remain to be answered," said WHO. "The outbreak in Ukraine
may be indicative of how the virus can behave in the northern hemisphere
during the winter season, particularly in health care settings typically
found in Eastern Europe."

"Many questions remain to be answered," said WHO. So far, only 5 of 86 deaths
have been confirmed as consequences of influenza pandemic (H1N1) 2009 virus infection.
Diagnostic facilities seem to be inadequate in Ukraine.

(Hold it.. wait.. BS ALERT: what about Baxter's lab, hmmm? Can't they test?  Or is WHO delaying acknowledgement of the Pneumonic plague; refusing to close the borders and praying for a fast SPREAD of this outside the Ukraine?)

How many of the half million people with respiratory illness in Ukraine are infected
by the pandemic (H1N1) 2009 virus remains unknown.
The outcome of WHO's investigation is awaited. - Mod.CP]

: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Satyagraha November 06, 2009, 05:07:28 PM

Quoting UberTrue

A summary of sorts...

This has to be the most under-reported event of the week.  Why has all mainstream US news outlets decided to completely ignore this story?

There is a massive outbreak of a seemingly more serious form of the swine flu (OR SOMETHING ELSE!) going on in Ukraine.

192,000 infected on Nov 2nd

The number of cases in Ukraine doubled in two days (almost 500,000 as of yesterday)

Some cases are seeing lungs fill up with blood (severe hemmorhagic pneumonia via a cytokine storm which was one of the main cause of fatalities in the very severe 1918 swine flu strain).  A cytokine storm causes the immune system of normally healthy adults to overreact causing severe illness or death (the healthier your immune system, the worse off you will be).

Reports mass acute respiratory problems in Lviv

Information on the 1918 flu

What makes this story very interesting is (1) a scientist warned of this back in August and was arrested right after and (2) reports from Ukraine of planes spraying something in the skies over cities just before things got really bad.

(1) According to Dr. True Ott, a man called him after an interview on his radio show on Aug. 11th stating that he had proof that Baxter was manufacturing a bioweaponized version of the flu vaccine in Ukraine that used RNA from the deadly 1918 flu.

Overview with some history on Baxter's past "mistakes"

Dr. Ott talking about the call with the man

Dr. Deagle discussing the incident

The next day Aug. 12th, this guy was chased down in LA for supposedly threatening the White House (read first two comments after the article as well).

Dr. Ott discusses Joseph Moshe's call on the Aug 17th Dr. Deagle show (6 minute mark of 2nd link)

2. (discusses Joseph Moshe at minute 6)

Another Dr. Deagle clip from Aug 10th (interesting they were saying the swine flu will begin producing more cytokine storms two months ago)

(2) Ukrainian citizens report aerial spraying on October 30th, right before the more serious form of the virus was being reported.

"Reports of helicopters and light airplanes spraying aerosols over Kiev, Lviv, Ternopil, and other cities throughout Ukraine are tonight flooding online forums and websites, hundreds of people have verified the reports with their own eye-witness accounts."

Ukrainian authorities are denying eyewitness reports of aerial spraying

Other related articles...

Ukraine to declare martial law?

Presidential address to Ukraine on Nov 4th

Vaccine opponents to be arrested in Ukraine

Another story on Joseph Moshe

Ukraine outbreak might be the plague

WHO arrives in Ukraine to study new flu

Someone made a short summary of these events in video form here

As usual, during the time of the outbreak there was a bioterrorism "exercise" going on...

Is it no surprise vaccine manufacturers are granted legal immunity?

Scare the public by saying there is a limited supply of vaccines...

...So they will eat the cookie
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: trailhound November 06, 2009, 05:42:32 PM
Heavy thread, marking for when get home. Spooky about the rapid rise of the 'new' flu on baxter's hometurf in the ukraine.
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Anti_Illuminati November 06, 2009, 07:46:48 PM

Flashback: CDC to Mix Avian, Human Flu Viruses in Pandemic Study
Published on 04-28-2009

Jan 14, 2004 – One of the worst fears of infectious disease experts is that the H5N1 avian influenza virus now circulating in parts of Asia will combine with a human-adapted flu virus to create a deadly new flu virus that could spread around the world.

That could happen, scientists predict, if someone who is already infected with an ordinary flu virus contracts the avian virus at the same time. The avian virus has already caused at least 48 confirmed human illness cases in Asia, of which 35 have been fatal. The virus has shown little ability to spread from person to person, but the fear is that a hybrid could combine the killing power of the avian virus with the transmissibility of human flu viruses.

Now, rather than waiting to see if nature spawns such a hybrid, US scientists are planning to try to breed one themselves—in the name of preparedness.

The Centers for Disease Control and Prevention (CDC) will soon launch experiments designed to combine the H5N1 virus and human flu viruses and then see how the resulting hybrids affect animals. The goal is to assess the chances that such a "reassortant" virus will emerge and how dangerous it might be.

CDC officials confirmed the plans for the research as described recently in media reports, particularly in a Canadian Press (CP) story.

Two ways to make hybrids
The plans call for trying two methods to create hybrid viruses, CDC spokesman David Daigle told CIDRAP News via e-mail. One is to infect cells in a laboratory tissue culture with H5N1 and human flu viruses at the same time and then watch to see if they mix. For the human virus, investigators will use A (H3N2), the strain that has caused most human flu cases in recent years, according to the CP report.

The other method is reverse genetics—assembling a new virus with sets of genes from the H5N1 and H3N2 viruses. Reverse genetics has already been used to create H5N1 candidate vaccines in several laboratories, according to Daigle. The National Institutes of Health (NIH) said recently it would soon launch a clinical trial of one of those vaccines.

Of the two methods, the co-infection approach was described as slower and more laborious, though closer to what happens in nature.

Any viable viruses that emerge from these processes will be seeded into animals that are considered good models for testing how flu viruses behave in humans, according to Daigle. The aim will be to observe whether the animals get sick and whether infected animals can infect others.

The World Health Organization (WHO) has been "pleading" for laboratories to do this research, because it could provide some evidence to back up the agency's warnings about the risk of a flu pandemic, according to the CP report.

Klaus Stohr, head of the WHO's global influenza program, was quoted as saying that if none of the hybrids caused disease, the agency might be inclined to dial down its level of concern. But if the experiments produce highly transmissible and pathogenic viruses, the agency will be more worried, he said.

Safety precautions
Because of the obvious risks in creating viruses with the potential to spark a pandemic, the work will be done in a biosafety level 3 (BSL-3) laboratory at the CDC in Atlanta, Daigle told CIDRAP News.

"We recognize that there is concern by some over this type of work. This concern may be heightened by reports of recent lab exposures in other lab facilities," he said. "But CDC has an incredible record in lab safety and is taking very strict precautions."

Daigle said the US Department of Agriculture requires that highly pathogenic avian influenza (HPAI) viruses be treated as "Select Agents" and that research on them must be done in BSL-3 labs with "enhancements." These include "special provisions to protect both laboratory workers and the environment."

BSL-3 is the second highest level of laboratory biosecurity. It is used for work with pathogens that may cause serious or potentially lethal disease if inhaled, such as tuberculosis or St. Louis encephalitis, according to the CDC.

CDC experiments with HPAI viruses have to pass reviews by the agency's Institutional Biosafety Committee and Animal Care and Use Committee, Daigle said. The facilities involved are inspected by the USDA and the CDC's Office of Safety and Health, and staff members who work with Select Agents require special clearance.

It's been done before
The upcoming experiments will not break entirely new ground for the CDC, the CP story revealed. The agency already has made hybrid viruses with H5N1 samples isolated from patients in Hong Kong in 1997, when the virus first caused human disease.

The results of that research have not yet been published, and the CDC has said little about them. In the CP report, Dr. Nancy Cox, head of the CDC's influenza branch, commented only, "Some gene combinations could be produced and others could not."

Daigle added little to that. He said, "The reassortment work with the 1997 isolate was intermittently interrupted with SARS [severe acute respiratory syndrome] and then the 2004 H5N1 outbreak. We are currently concentrating our efforts on understanding the pathogenicity of the 2004 strains (non-reassortants) in mammalian models."

He said the CDC hopes to prepare a report on that research "in the near future."

See also:

CDC information on biosafety levels

Archive Number   20070519.1602
Published Date   19-MAY-2007
Subject   PRO/AH/EDR> Avian influenza, human (81): factfile

A ProMED-mail post
ProMED-mail is a program of the
International Society for Infectious Diseases

Date: Wed 16 May 2007
Source: CIDRAP, Wed 16 May 2007 [edited]

Avian influenza (bird flu): implications for human disease
[A comprehensive reference document covering all aspects of the biology of
human avian influenza H5N1 virus updated to 16 May 2007 is available at the
CIDRAP (Center for Infectious Disease Research and Policy, University of Minnesota) website via the general link:
The contents are arranged under the following headings and include
references to key publications:
Laboratory testing for avian influenza in humans
Summary of avian influenza in humans
Current outbreak of H5N1 in birds and other animals
H5N1 in humans: epidemiologic features
H5N1 in humans: clinical features
Treatment and prophylaxis
Current status of H5N1 candidate vaccines
Current WHO and CDC travel recommendations
Use of seasonal flu vaccine in humans at risk for H5N1 infection
Surveillance considerations
Influenza pandemic considerations
Infection control recommendations
Guidance to protect workers from avian influenza viruses
Food safety issues
The following sections are reproduced in full to give a flavour of the
content of the document, which uniquely attempts to cover the whole field
of the interaction of avian H5N1 influenza viruses with the human population.
The Agent
Avian influenza is caused by influenza A viruses. More information about
avian influenza in bird populations can be found in the document “Avian
Influenza (Bird Flu): Agricultural and Wildlife Considerations” on this site.
•   Family: Orthomyxoviridae
•   Enveloped virions are 80 to 120 nm in diameter and 200 to 300 nm long and
may be filamentous.
•   They consist of spike-shaped surface proteins, a partially host-derived
lipid-rich envelope, and matrix (M) proteins surrounding a helical
segmented nucleocapsid (6 to 8 segments).
•   The family contains 5 genera, classified by variations in nucleoprotein
(NP and M) antigens: influenza A, influenza B, influenza C, thogotovirus,
and isavirus.
•   Genus: Influenzavirus A
•   Consists of a single species: influenza A virus.
•   Influenza A viruses are a major cause of influenza in humans.
•   All past influenza pandemics have been caused by influenza A viruses.
•   The multipartite genome is encapsidated, with each segment in a separate
nucleocapsid. A total of 8 different segments of negative-sense
single-stranded RNA are present; this allows for genetic reassortment in
single cells infected with more than one virus and may result in multiple
strains that are different from the initial ones (see References: Voyles
•   The genome consists of 10 genes encoding for different proteins (8
structural proteins and 2 nonstructural proteins). These include the
following: 3 transcriptases (PB2, PB1, and PA), 2 surface glycoproteins
(hemagglutinin [HA] and neuraminidase [NA]), 2 matrix proteins (M1 and M2),
one nucleocapsid protein (NP), and 2 nonstructural proteins (NS1 and NS2).
•   The virus envelope glycoproteins (HA and NA) are distributed evenly over
the virion surface, forming characteristic spike-shaped structures.
Antigenic variation in these proteins is used as part of the influenza A
virus subtype definition (but not used for influenza B or C viruses).
•   Influenza A virus subtypes:
•   There are 16 different HA antigens (H1 to H16) and 9 different NA
antigens (N1 to N9) for influenza A. Until recently, 15 HA types had been
recognized, but a new type (H16) was isolated from black-headed gulls
caught in Sweden and the Netherlands in 1999 and reported in the literature
in 2005 (see References: Fouchier 2005).
•   All known subtypes of influenza A can be found in birds, and wild aquatic
birds are the major reservoir for influenza A viruses (see References:
Fouchier 2004).
•   Human disease historically has been caused by 3 subtypes of HA (H1, H2,
and H3) and 2 subtypes of NA (N1 and N2). H1 and H3 are the subtypes that
currently cause seasonal influenza in human populations around the globe
each year.
•   More recently, human disease has been recognized to be caused by
additional HA subtypes, including H5, H7, and H9. Such cases have
predominantly been associated with exposure to infected birds.
Person-to-person transmission has occurred in a few isolated situations.
•   Other mammalian hosts for influenza A
•   Influenza A viruses have traditionally been known to cause disease in
horses, pigs, whales, and seals.
•   H5N1 influenza A has now been shown to infect cats, leopards, tigers,
civets and possibly dogs (see References: European Centre for Disease
Prevention and Control Influenza Team 2006: H5N1 infections in cats;
Keawcharoen 2004; Kuiken 2004; Songserm 2006; Thanawongnuwech 2005; Webster
2006; Yingst 2006; and see Aug 31, 2006,
CIDRAP News story).
A recent report involving cats experimentally infected with H5N1
demonstrated that infected cats excreted the virus via the respiratory
tract and the digestive tract, suggesting that in addition to the
respiratory route, other routes of transmission may play a role in spread
among mammalian hosts (see References: Rimmelzwaan 2006).
•   Cases of canine influenza caused by H3N8 recently have been recognized in
the United States; this subtype traditionally has been found in horses (see
References: Crawford 2005, Yoon 2005).
•   Avian influenza
•   The term “avian influenza” is used to describe influenza A subtypes that
primarily affect chickens, turkeys, guinea fowls, migratory waterfowl, and
other avian species.
•   “Avian influenza” is an ecological classification that does not
correspond exactly to other classification schemes.
•   Severe disease from influenza generally does not develop in wild birds;
however, recently H5N1 has been shown to be virulent for wild bird species.
An outbreak of H5N1 among migratory geese and other wild birds in Qinghai
province, China, was identified in May 2005 (see References: Chen 2005, Liu
2005). An outbreak in wild swans occurred in Azerbaijan in February 2006,
and severe illness from H5N1 influenza has been recognized in a variety of
other wild bird species (see References: Gilsdorf 2006; Olsen 2006; USGS
National Wildlife Health Center).
•   Outbreaks of influenza have been recognized in domestic poultry (chickens
and turkeys) for many years. Avian influenza strains in domestic chickens
and turkeys are classified according to disease severity, with 2 recognized
forms: highly pathogenic avian influenza (HPAI), also known as fowl plague,
and low-pathogenic avian influenza (LPAI). Avian influenza viruses that
cause HPAI are highly virulent, and mortality rates in infected flocks
often approach 100 per cent. LPAI viruses are generally of lower virulence,
but these viruses can serve as progenitors to HPAI viruses. All HPAI
strains identified to date have involved H5 and H7 subtypes.
•   Human infections caused by avian strains have been associated with both
HPAI and LPAI strains (H5, H7, and H9) (see References: HHS 2005: Pandemic
influenza plan).
•   Evidence that HPAI strains arise from LPAI strains has led the World
Organization for Animal Health (OIE) to classify all H5 or H7 strains as
notifiable (see References: Alexander 2003, Capua 2004, OIE 2005).
•   In the United States, currently only HPAI avian strains and reconstructed
1918 H1N1 strains are regulated as select agents (see Biosafety and
Biosecurity, below).
•   The 1918 influenza pandemic strain (H1N1) appears to be of avian origin
(see References: CDC: Information about pandemic influenza viruses). The
pandemic strains of 1957-58 (H2N2) and 1968-69 (H3N2) both involved
reassortment events between avian and human influenza strains.
•   H5 subtypes
•   H5 subtypes can be found throughout the world and include both LPAI and
HPAI strains.
•   H5N1 is responsible for the current panzootic among domestic poultry and
other birds in Asia, Europe, and Africa.
•   Recent genetic characterization of H5N1 strains involved in the current
panzootic has demonstrated 2 distinct phylogenetic clades (see References:
Webster 2006; WHO Global Influenza Program Surveillance Network; WHO:
Antigenic and genetic characteristics of H5N1 viruses and candidate H5N1
vaccine viruses developed for potential use as prepandemic vaccines). Clade
1 viruses have circulated primarily in Cambodia, Thailand, and Vietnam, and
clade 2 viruses have circulated primarily in China and Indonesia and have
spread westward to the Middle East, Europe, and Africa. A total of 6
different subclades of clade 2 have been recognized; 3 of these are
primarily responsible for recent human H5N1 cases. The most recent wave of
outbreaks in Thailand (in July 2006) has been caused by viruses closely
related to those that caused outbreaks in Thailand in 2004-2005 and to
viruses recently circulating in southeast China (see References:
Chutinimitkul 2007).
•   H7 and H9 subtypes
•   H7 includes HPAI and LPAI strains.
•   H9 is only known to include LPAI strains.
•   These subtypes have caused infections in humans on rare occasions (see
References: CDC: Avian influenza A viruses; NIAID: Timeline of human
•   Influenza A nomenclature
•   Antigenic strain nomenclature is based on: (1) host of origin (if other
than human), (2) geographic origin, (3) strain number, (4) year of
isolation, and (5) HA and NA type. Examples (for human strains) include:
A/Hong Kong/03/68[H3N2], A/swine/Iowa/15/30[H1N1]).
•   As with other influenza A subtypes, standard nomenclature is used to name
avian strains (eg, A/Chicken/HK/5/98 [H5N1]).
•   Physical characteristics of influenza A viruses
•   Viruses remain infectious after 24 to 48 hours on nonporous environmental
surfaces and less than 12 hours on porous surfaces (see References: Bean
1982). (Note: The importance of fomites in disease transmission has not
been determined.)
•   Influenza A viruses can persist for extended periods of time in water
(see References: WHO: Review of latest available evidence on risks to human
health through potential transmission of avian influenza [H5N1] through
water and sewage). One study of subtype H3N6 found that virus resuspended
in Mississippi River water was detected for up to 32 days at 4 deg C [39.2
deg F] and was undetectable after 4 days at 22 deg C [71.6 deg F] (see
References: Webster 1978). Another study found that several avian influenza
viruses persisted in distilled water for 207 days at 17 deg C [62.6 deg F]
and 102 days at 28 deg C [82.4 deg F] (see References: Stallknecht 1990).
•   Recent data from studies of H5N1 in domestic ducks have shown that H5N1
can survive in the environment for 6 days at 37 deg C [98.6 deg F] (see
References: WHO: Laboratory study of H5N1 viruses in domestic ducks).
•   Inactivation of the virus occurs under the following conditions (see
References: OIE 2002, PHS): temperatures of 56 deg C [132.8 deg F] for 3
hours or 60 deg C [140 deg F] or more for 30 minutes; acidic pH conditions;
presence of oxidizing agents such as sodium dodecyl sulfate, lipid
solvents, and B-propiolactone; and exposure to disinfectants such as
formalin and iodine compounds.
Laboratory testing for avian influenza in humans
General considerations
•   Tests for influenza include: viral culture, polymerase chain reaction
(PCR), rapid antigen testing, and immunofluorescence.
•   Laboratory tests are widely used to identify influenza virus at the genus
level (influenza A/B) or at the H-type level (H1, H3, and H5).
•   H subtype-specific tests must be used to identify potential avian
strains, including H5N1.
•   The World Health Organization (WHO) recommends forwarding all H5, H7, and
H9-positive isolates to a designated influenza reference laboratory for
confirmation and N-typing (see References: WHO: Guidelines for global
surveillance of influenza A/H5; WHO: Recommended laboratory tests to
identify avian influenza A virus in specimens from patients with an
influenza-like illness).
•   Serologic tests have been used to diagnose infection retrospectively.
•   During a pandemic alert period for an avian influenza virus, patients who
meet certain criteria (such as influenza symptoms and recent travel to an
area affected by a novel strain) should be considered for laboratory testing.
•   During a pandemic (involving an avian strain or other strain),
recommendations for laboratory testing may be somewhat unique and dependent
upon factors such as: (1) availability of reagents and laboratory surge
capacity, (2) the presence or absence of other influenza strains in the
community, (3) level of influenza activity in the community, and (4)
treatment considerations.
•   The sensitivity and specificity of laboratory tests appears to vary with
the involved strain, which has implications for avian influenza and other
emerging influenza variants (see References: Weinberg 2005).
•   Laboratory tests are required for specific identification of avian
influenza. The most likely ways that an avian influenza strain would be
detected in the human population are:
•   Outbreak investigations or investigation of unexplained death in a
previously healthy individual
•   Influenza surveillance with laboratory testing
•   Investigation of unusual laboratory findings
•   Testing of persons with influenza-like symptoms who meet certain exposure
•   Laboratory-based influenza surveillance networks
•   WHO Global Influenza Surveillance Network (see References)
•   CDC National Respiratory and Enteric Virus Surveillance System (NREVSS)
(see References)
•   State or local surveillance health department surveillance networks

Specimen collection
The following information is taken from a field operations guide for H5N1
influenza that was released by WHO in early November 2006 (see References:
WHO 2006: Collecting, preserving, and shipping specimens for the diagnosis
of avian influenza A [H5N1] virus infection). Information also was taken
from the HHS Pandemic Influenza Plan where noted (see References: HHS 2005:
Pandemic influenza plan [Part 2, Supplement 2]).
Specimens to collect from suspect cases
•   Upper respiratory tract
•   Posterior-pharyngeal (throat) swabs (provide the highest yield)
•   Nasal swabs with nasal secretions (from the anterior turbinate areas) or
nasopharyngeal aspirates or swabs (these specimens are more appropriate for
seasonal influenza and the yield may be lower for avian influenza)
•   Lower respiratory tract:
•   A tracheal aspirate or bronchoalveolar lavage specimen (if the patient is
•   Blood:
•   Serum (acute and convalescent if possible)
•   Secondary specimens:
•   Plasma in EDTA (for detection of viral RNA)
•   Rectal swab (for patients with diarrhea)
•   Spinal fluid (if meningitis is suspected and a spinal tap is performed
for diagnostic purposes)
•   Pleural tap fluid (referred to in the HHS Plan)
•   Autopsy specimens (referred to in the HHS Plan)

When to collect specimens from suspect cases
•   Ideally, a throat swab should be taken within 3 days after illness onset;
if initial specimens are negative, but a high index of suspicion remains,
testing should be repeated as soon as possible. (According to the HHS Plan,
specimens optimally should be collected within 4 days after illness onset.)
•   Virus may be detected in tracheal aspirates from onset of lower
respiratory symptoms until the 2nd or 3rd week of illness.
•   An acute phase serum sample should be taken 7 days or less after symptom
onset and a convalescent sample should be taken 3 to 4 weeks following
illness onset.
•   Single serum samples should be collected 14 days or later after symptom
•   Serum or plasma for detecting viral RNA should be obtained during the
first 7 to 9 days after symptom onset.
•   Ideally specimens should be collected before antiviral therapy, but
treatment should not be delayed in order to take specimens.
•   Specimens should be collected from deceased patients as soon as possible
after death.
Specimen collection and transport
•   Detailed methods for specimen collection and transport are provided in
the WHO field guide (see References: WHO 2006: Collecting, preserving, and
shipping specimens for the diagnosis of avian influenza A [H5N1] virus
•   Infection control precautions should be consistently observed during
specimen collection.
•   Only sterile dacron or rayon swabs with plastic shafts should be used.
Calcium alginate or cotton swabs or swabs with wooden sticks should not be
used (or used only when appropriate swabs are not available).
•   Viral transport media (VTM) should be used for nasopharyngeal and
oropharyngeal swabs and, according to the HHS Plan, specimens should be
maintained at refrigerator temperature (4 deg C [39.2 deg F] to 8 deg C
[46.4 deg F]) until testing is performed. Freezing at 70 deg C [158 deg F]
is best for maintaining viability during extended storage.
•   According to the HHS Plan, with regard to autopsy specimens, large
airways have the highest yield for immunohistochemistry (IHC) tests. A
total of 8 blocks or fixed-tissue specimens from each of the following
sites should be obtained. Fixed tissue should be transported at room
temperature (not frozen); fresh unfixed tissue should be frozen.
•   Central (hilar) lung with segmental bronchi
•   Right and left primary bronchi
•   Trachea (proximal and distal)
•   Representative pulmonary parenchyma from right and left lung

Biosafety and biosecurity
New safety rules and recommendations for influenza virus will be published
in a revised edition of Biosafety in Microbiological and Biomedical
Laboratories (BMBL) (see References: CDC: Interim CDC-NIH recommendation
for raising the biosafety level for laboratory work involving
noncontemporary human influenza [H2N2] viruses; CDC: Update on influenza A
[H5N1] and SARS: Interim recommendations for enhanced U.S. surveillance,
testing, and infection controls; HHS 2005: Pandemic influenza plan).
Current recommendations for interpandemic and pandemic alert periods include:
•   Culture of influenza subtypes H1-4, H6, and H8-15 (with exceptions noted
below) and culture of specimens from patients not suspected of having novel
influenza strains requires BSL-2 containment and practices (Animal BSL-2
for animal models).
•   Culture of noncontemporary influenza strains (H2N2) or research involving
reverse genetics of the 1918 Spanish flu strain (H1N1) requires BSL-3
facilities and Animal BSL-3 practices, including containment with rigorous
adherence to additional respiratory protection and clothing change
protocol, use of negative pressure, high-efficiency particulate air (HEPA)
filtered respirators or positive air-purifying respirators (PAPRs), use of
HEPA filtration for treatment of exhaust air, and amendment of personnel
practices to include personal showers prior to exiting the laboratory.
•   Culture from patients suspected of having avian influenza, other novel
influenza strains, or severe acute respiratory syndrome (SARS) coronavirus
should only be conducted under enhanced BSL-3 containment (also see
Biosecurity below). This includes controlled access, double-door entry with
changing room and shower, use of respirators, decontamination of all waste,
and showering out of all personnel. These diagnostic activities must be
kept separate from routine influenza diagnostic activities (e.g., probable
H1 or H3 isolates) to prevent recombination.
•   Indirect immunofluroescence (IFA) of specimens requires BSL-2 containment
and practices. Culture biocontainment recommendations should be implemented
when IFA is used for culture identification.
•   Direct detection methods, including commercial antigen detection assays
and reverse transcriptase polymerase chain reaction (RT-PCR), should be
conducted under BSL-2 with a Class II biological safety cabinet. Serologic
methods require BSL-2 containment.
•   If H5N1 avian influenza virus is presumptively identified by one of the
above direct methods, further work should be conducted using the enhanced
BSL-3 procedures described for culture.
•   Any new or re-emergent human influenza strain with suspected pandemic
potential should be treated in the same manner as described for H5N1 avian
•   Additional requirements and recommendations apply for laboratory work
involving live animals.
•   Biosecurity
•   Human influenza strains, with a few exceptions (see below), are not
regulated as select agents. Inclusion of potentially pandemic strains on
the select agent list is currently under consideration (see References:
CDC: Interim CDC-NIH recommendation for raising the biosafety level for
laboratory work involving noncontemporary human influenza [H2N2] viruses;
CDC: Update on avian influenza A[H5N1] and SARS). Despite the absence of
regulatory authority, standard biosecurity measures should be maintained
for potentially pandemic strains.
•   The USDA classifies HPAI as an agricultural select agent regulated under
7 CFR Part 331 and 9 CFR Part 121 of the Federal Register, which was
published as an Final Rule in the 18 Mar 2005, issue (see References:
USDA/APHIS: Agricultural Bioterrorism Protection Act of 2002). Laboratories
that work with HPAI strains (H5 or H7) or perform diagnostic cultures for
suspected human cases of avian influenza caused by H5 or H7 or suspected
cases of SARS must be registered with the USDA.
•   Both registered and exempt laboratories that identify a select agent
contained in a specimen presented for diagnosis, verification, or
proficiency testing must secure the agent against theft, loss, or release
until transfer or destruction. Unregistered laboratories must transfer or
destroy select agents within 7 days of identification. Any theft, loss, or
release of the agent must be reported to the select agent authority (see
References: USDA/APHIS: Questions and answers).
Virus isolation by cell culture
•   Virus isolation is considered the “gold standard” of influenza testing
(see References: Hayden 2002, Treanor 2005).
•   Culture of specimens from suspect cases of avian influenza requires
special containment facilities, procedures, and registration (see above).
Samples from cases without specific risk factors may be cultured using
standard facilities and procedures.
•   Unlike antigen or nucleic acid�based tests, a positive result is
considered definitive for the diagnosis.
•   Cell culture measures growth rather than the presence or absence of
specific targets. As cell lines are designed to support the growth of a
wide range of viruses, cell culture will likely allow for detection of
emerging and pandemic influenza strains (see References: Australian
Government Department of Health and Ageing).
•   Isolates obtained from cell culture are required for strain
characterization, which is an integral part of global influenza
surveillance and monitoring activities during a pandemic (see References:
HHS 2005: Pandemic influenza plan).
•   Cell culture is subject to certain restrictions (see Biosafety and
Biosecurity above).
•   Specimens for culture optimally should be collected within 3 days after
illness onset.
•   Turnaround time for the standard method is 2 to 14 days.
•   Culture consists of growth on a cell monolayer, detection of viral
growth, and specific identification.
•   Virus detection and identification methods for standard culture include
the following:
•   Cell lines include Madin-Darby canine kidney (MDCK), primary rhesus
monkey kidney (PRMK), or cynomolgus monkey kidney. Other cell lines, such
as Vero, mink lung, and MRC-5, also support growth of influenza virus if
trypsin is incorporated into serum-free medium.
•   Cytopathic effect (CPE) is not a consistent feature of influenza A virus.
If present, CPE is nonspecific, including vacuolization or cell degeneration.
•   Assays for haemadsorption (HAd) (ie, influenza-infected cells bind red
blood cells [RBCs]) are performed blindly, typically at 7 and 14 days or on
cells exhibiting CPE. Other viruses, such as parainfluenza and mumps
viruses, may also cause haemadsorption. The lack of HAd specificity may be
an advantage in detecting new or pandemic strains.
•   Hemagglutination inhibition (HI or HAI) is used to identify the viral
subtype. Cell supernatant is mixed with RBCs; identification is by
quantitative inhibition of agglutination using subtype-specific antisera.
Homologous strains yield high HI titers. New pandemic strains would likely
be Had-positive with or without CPE, with low or negative titers to group
specific antisera.
•   Identification of infected cells is by direct or indirect
immunofluorescence (e.g., DFA, IFA), enzyme-linked immunoassays (EIA), or
PCR-based methods. Assays with more conserved, less specific targets are
more likely to detect newly emerged strains.
•   The time to detection in culture, as measured in one study conducted
during two influenza seasons, ranged from 5 days (>90 percent of positive
specimens) to 7 days (100 percent of positive specimens) (see References:
Newton 2002).
•   A golden rule of laboratory testing is to never process clinical
specimens from humans and swine (and presumably birds) in the same
laboratory (see References: WHO recommended laboratory tests to identify
influenza A/H5 in specimens from patients with an influenza-like illness).
•   Shell vial assay (rapid culture), when combined with a rapid
detection/identification method, offers a sensitive and rapid diagnostic
alternative to standard culture. This method does not result in an adequate
viral titer or volume for further characterization and would thus not be
appropriate for pandemic influenza surveillance without subculture.
Direct detection methods
Direct detection methods do not result in production of an isolate and
would be inadequate for surveillance or definitive characterization of
pandemic strains. Nevertheless, owing to their relatively rapid turnaround
time, safety, and stability, direct detection methods play an important
role in pandemic influenza preparedness.
•   RT-PCR assays
•   RT-PCR assays use conserved targets such as the matrix (M) protein for
genus-level identification. Hemagglutinin and neuraminidase targets are
used for specific identification of avian subtypes. PCR generally is not
used for strain-level identification, which is based on serologic markers.
•   The sensitivity of RT-PCR has been reported to be in the range of 90
percent to 100 percent when compared with cell culture; however, several
researchers have reported significantly higher numbers of total positive
specimens with RT-PCR, possibly reflecting its ability to detect nonviable
virions (see References: Coiras 2003, Hayden 2002, Herrmann 2001, Pachucki
2004, Wallace 1999).
•   On 3 Feb 2006, the Food and Drug Administration (FDA) announced clearance
of an Influenza A/H5 (Asian Lineage) Virus Real-Time Reverse
Transcription�Polymerase Chain Reaction (RT-PCR) Primer and Probe Set and
inactivated virus as a source of positive RNA control for the in vitro
detection of highly pathogenic influenza A/H5 virus (Asian lineage) (see
References: CDC 2006: New laboratory assay for diagnostic testing of avian
influenza A/H5 [Asian lineage]). These reagents and assay protocols have
been distributed by CDC to state and city LRN (Laboratory Response Network)
laboratories. Testing with the new assay is limited to LRN-designated
•   Multiplex real-time RT-PCR assays have been developed for specific
detection of H5N1 (See References: Kessler 2004, Ng 2005, Payungporn 2005).
•   While culture of specimens from possible avian influenza (H5N1) cases is
not recommended without strict containment and specific registration
(described above), RT-PCR can be conducted using BSL-2 facilities and
practices (see References: HHS 2005: Pandemic influenza plan).
•   Common PCR targets include the matrix (M) protein (for genus-level
identification), hemagglutinin, and neuraminidase (for subtype-level
identification). PCR generally is not used for strain-level identification,
which is based on serologic markers.
•   The likelihood that a RT-PCR assay will detect new pandemic strains
increases when more conserved target sequences are used.
•   As with other PCR-based assays, efforts should be made to minimize and
detect amplicon contamination.
•   Samples positive by RT-PCR for a novel influenza subtype should be
forwarded to a public health laboratory (if testing was conducted at a
private laboratory) or to CDC for confirmation (see References: HHS 2005:
Pandemic influenza plan).
•   The development of portable real-time platforms has made possible the use
of PCR assays in the field (see References: Perdue 2003).
•   Immunofluorescence
•   IFA methods may be used to identify influenza to the species level
(influenza A or B) or specific H subtypes (including H5) directly from
specimens or cell culture. CDC distributes IFA typing and subtyping
reagents to WHO-collaborating laboratories, including many health
department laboratories. If HPAI strains are suspected, enhanced BSL-3
containment should be used (see References: WHO: Recommended laboratory
tests to identify avian influenza A virus in specimens from humans; FDA:
Cautions in using rapid tests for detecting influenza A viruses; HHS 2005:
Pandemic influenza plan).
•   Direct immunofluorescence (DFA) methods are faster and less labor
intensive than IFA but are less sensitive and are currently only available
for genus-specific detection (see other rapid direct tests in the next
•   Molecular microarray tests using flow-through chip technology
•   A molecular microarray for influenza typing and subtyping using a
flow-thru chip platform was initially described in 2004 (see References:
Kessler 2004).
•   There were 2 reports released in August 2006 which involved a study of
the FluChip-55 diagnostic microarray and showed that the test could be a
valuable tool in identifying influenza viruses (see References: Mehlmann
2006, Townsend 2006). The FluChip used in the study contained 55 sequences
of RNA representing a variety of type A and type B flu viruses, including
H3N2, H1N1, and H5N1. Combined results after 2 rounds of testing showed
that the FluChip allowed users to obtain correct information about both
type and subtype from 72 percent of 72 samples tested. Full information on
type, but only partial information on subtype, was obtained for an
additional 13 percent of the samples, while 10 percent of the samples could
be identified by type only (no information about subtype). The entire
analysis time was less than 12 hours.
•   Scientists recently have developed an improved microarray test referred
to as the �MChip,� which has several advantages over the FluChip. While the
FluChip is based on 3 influenza genes�hemagglutinin (HA), neuraminidase
(NA) and matrix (M)�the MChip is based on only the M gene segment, which
mutates much less rapidly. A recent evaluation demonstrated that the assay
exhibited a clinical sensitivity of 97 percent and clinical specificity of
100 percent (see 15 Nov 2006,
CIDRAP News Story).
•   Other rapid direct tests (see References: Call 2005; CDC: Interim
guidance for influenza diagnostic testing during the 2004-05 influenza
season; Treanor 2005; WHO: Checklist for influenza pandemic preparedness
•   Rapid tests detect viral antigen (generally nucleoprotein) or enzymatic
activity (neuraminidase) directly on patient specimens using a variety of
•   Rapid tests are designed to identify influenza A only, influenza A or B
without identifying the type, or influenza A or B with type-specific
•   Reported sensitivities range from 40 percent to 80 percent.
•   Sensitivity is generally greater in children than adults.
•   Sensitivity is greater early in the course of illness.
•   Rapid test predictive value and disease prevalence: The predictive value
of rapid assays without confirmation by a reference test is strongly
correlated with disease prevalence in the community, as is clinical
diagnosis without laboratory testing. When the disease prevalence is low,
the tests’ positive predictive value decreases and positive results should
be confirmed by culture or RT-PCR. When influenza is known to be
circulating (i.e., high prevalence in the community), the negative
predictive value is lower and clinicians should consider confirming
negative tests with viral culture or other tests.
•   Rapid test predictive value and diagnostic indications: Rapid tests
increase the diagnostic predictive value when used for confirmation of
influenza (when symptoms are strongly suggestive) and for ruling out
influenza (when symptoms suggest illness other than influenza). When
symptoms are not strongly suggestive in either direction, the utility of
rapid testing becomes questionable.
•   While the sensitivity and specificity of rapid tests has been evaluated
for circulating strains, these measures are largely unknown for detection
of emerging strains (including pandemic strains) (see References: FDA:
Cautions in using rapid tests for detecting influenza A viruses). Only 4
(36 percent) of 11 culture-positive H5N1 influenza A specimens from
patients in Thailand were positive by rapid antigen tests (see References:
WHO Writing Committee of WHO Consultation on Human Influenza A/H5 2005).
•   WHO, in their Checklist for Influenza Pandemic Preparedness Planning,
recommends against routine use of commercial rapid antigen detection kits
and suggests they be used for outbreak investigation only when no other
options exist (see References: WHO Writing Committee of WHO Consultation on
Human Influenza A/H5 2005).
Serologic testing can be used for retrospective diagnosis of infection but
is rarely useful for patient management and is not widely available (see
References: Hayden 2002; Treanor 2005; HHS 2005: Pandemic influenza plan).
•   Acute-phase sera should be collected within 1 week after illness onset
and convalescent sera should be collected 2 to 3 weeks later.
•   The most common serologic methods are complement fixation (CF), HAI, and
enzyme immunoassays (EIA). A variety of other methods, such as
neutralization, microneutralization, single radial hemolysis, radial
immunodiffusion, and Western blot, have been reported (see References:
Hayden 2002, Rowe 1999).
•   IgG, IgA, and IgM antibodies appear simultaneously about 2 weeks after
initial infection. Antibodies appear more quickly with subsequent
infections. Tests for IgM and IgA are less useful than IgG for routine
clinical use, as most infections are reinfections (see References:
Australian Government Department of Health and Ageing; Hayden 2002).
•   Peak antibody response occurs 4 to 7 weeks after infection.
•   Since most people are repeatedly exposed to influenza viruses, a 4-fold
rise in titer between acute and convalescent sera generally is considered
necessary for confirmation of influenza infection.
•   While paired sera are optimal, single convalescent specimens may be
useful in investigations involving novel viruses. Antibody test results
have been compared with results from age-matched persons in the acute phase
of illness or from non-ill controls. The geometric mean titers between the
two groups to a single influenza virus type or subtype can be compared (see
References: HHS 2005: Pandemic influenza plan).
•   HAI EIAs measure antibody to hemagglutinin. These tests are more
sensitive than CF, but their increased specificity appears to limit their
ability to detect new strains.
•   HAI titers of at least 1:40 or serum neutralizing titers of 1:8 or
greater are associated with protection.
•   HAI titers in human avian influenza cases have been low or undetectable
(see References: HHS 2005: Pandemic influenza plan).
•   CF measures antibody response to nucleoprotein, which is conserved among
influenza A strains. This feature could be an advantage for diagnosis of
infection with novel pandemic strains.
•   The microneutralization assay can sensitively and specifically detect
H5N1 antibody in patients with H5N1 influenza. Since the test uses
infectious organisms, HPAI strains should be tested under enhanced BSL-3
containment. As with other tests, paired sera are preferable to single
specimens (see References: HHS 2005: Pandemic influenza plan).
Susceptibility testing
Susceptibility testing generally is conducted at specialized laboratories
as part of surveillance or research and is considered an integral component
of pandemic influenza response.
•   Plaque reduction assay (see References: Hayden 1980, McKimm-Breschkin 2003)
•   The traditional influenza susceptibility testing method for the M2 ion
channel inhibitors (amantadine, rimantadine)
•   Can detect a wide range of resistance phenotypes
•   Limited utility for neuraminidase inhibitors
•   Enzyme inhibition assays (see References: McKimm-Breschkin 2003,Wetherall
•   Useful for assay of neuraminidase inhibitors
•   Chemiluminescent or fluorescent substrates
•   Sequence analysis (see References: McKimm-Breschkin 2003,Wetherall 2003)
•   Used to detect mutations in genes known or suspected to be responsible
for resistance.
•   Neuraminidase gene sequences from strains isolated prior to introduction
of the drugs can be used to evaluate current strain sequences.
•   Mutations in the M2 can be used to detect amantadine resistance (see
References: Pachucki 2004).
•   Researchers have recently reported a PCR assay to efficiently and
accurately detect oseltamivir-sensitive and oseltamivir resistant H5N1
strains (see References: Suwannakarn 2006). The assay is based on the fact
that oseltamivir resistance is caused by a single amino acid substitution
from histidine (H) to tyrosine (Y) at position 274 of the neuraminidase
active site.
•   The Neuraminidase Inhibitor Susceptibility Network (NISN) was established
to monitor susceptibility of clinical isolates to zanamivir and
oseltamivir. The chemiluminescent neuraminidase enzyme assay was chosen by
the NISN as the method of choice for testing neuraminidase inhibitors (see
References: Wetherall
Summary of avian influenza in humans
In the past several years, it has become clear that avian influenza viruses
can infect humans. Situations where avian influenza virus subtypes have
been recognized to be transmitted to humans and cause disease. This section
comprises a tabulation of avian influenza in humans during the period 1997
to 2004.
Current outbreak of H5N1 in birds and other animals
The outbreak of HPAI caused by a strain of H5N1 avian influenza started in
Asia in the fall of 2003 and spread in domestic poultry farms at an
historically unprecedented rate. The outbreak tapered off in spring 2004
but in summer re-emerged in several countries in Asia (including Cambodia,
China, Lao People’s Democratic Republic [PDR], Thailand, and Vietnam),
where it is ongoing. The H5N1 strains currently causing outbreaks across
Asia and elsewhere are genetically distinct from the strain isolated from
humans in Hong Kong in 1997. Since January 2002, the predominant avian H5N1
strain in southern China has been genotype Z. Since its emergence, this
strain has replaced other genotypes and has become the predominant genotype
circulating in aquatic and terrestrial poultry in the region (see
References: Li 2004). Ongoing market surveillance in China demonstrates
that a single sublineage of genotype Z (Fujian [FJ]-like) has emerged in
poultry in China since late 2005 (see References: Smith 2006). A 2006 study
suggests that the H5N1 virus has been circulating in southern China for
nearly a decade (see References: Chen 2006).
In the summer of 2005, H5N1 began expanding its geographic range beyond
Asia; this trend has continued into 2007. This section comprises a
comprehensive listing of the outbreaks of H5N1 avian influenza virus
infection. As of August 2006, more than 220 million birds have been killed
by the virus or culled to prevent further spread (see References: FAO:
Caucasus, Balkins at high risk for deadly H5N1 virus), and the number keeps
growing. Areas currently affected by H5N1 avian influenza in poultry or
migratory birds are shown in the following table.
Countries Affected by H5N1 in Poultry and Wild Birds as of 3 May 2007: East
Asia, Southeast Asia Europe Siberia, Central Asia, Middle East Africa
Cambodia China Hong Kong Indonesia Japan Lao DPR Malaysia Myanmar Mongolia
South Korea Thailand Vietnam Albania Austria Bosnia-Herzegovina Bulgaria
Croatia Czech Republic Denmark England France Germany Greece Hungary Italy
Poland Romania Russia (European Russia) Scotland Serbia Slovakia Slovenia
Spain Sweden Switzerland Afghanistan Azerbaijan Bangladesh Cyprus Georgia
(former Soviet republic) India Iran Iraq Israel Jordan Kazakhstan Kuwait
Pakistan Palestine Turkey Ukraine Russia (Siberia) Saudi Arabia Burkina
Faso Cameroon Djibouti Egypt Ghana Ivory Coast Niger Nigeria Sudan.
Information taken from FAO (see References: FAO 2006: Should wild birds now
be considered a permanent reservoir of the virus?) and current news reports
If H5N1 continues to circulate widely among poultry, the potential for
emergence of a pandemic strain remains high. For example, H5N1 viruses have
been found in pigs in southern China in 2001 and 2003 (see References:
Cyranoski 2004), and human H3N2 influenza viruses are endemic in pigs in
that area. H5N1 has been reported in pigs in Indonesia as well (see Oct 10,
CIDRAP News Story and see References: Cyranoski 2005).
Thus, the conditions exist for exchange of genetic material between the
different viruses in the pig host (see References: Li 2004; WHO: Avian
influenza: update: implications of H5N1 infections in pigs in China). Some
scientists believe that reassortment between an avian and a human strain
could occur in the human population without an intermediary host; if this
proves true, as more humans become exposed and infected, the potential for
reassortment with a human strain may also increase. It is also possible
that a pandemic strain could emerge following a more gradual process of
adaptive mutation in humans, which is likely what happened with the 1918
H1N1 pandemic strain (see References: Taubenberger 2005; WHO: Influenza
pandemic preparedness and response 2005).
Domestic cats recently have been shown to be susceptible to H5N1 infection
and some experts are concerned that cats could play a role in transmission
of H5N1 to humans, although this has not been documented to date (see
References: Kuiken 2006). Asymptomatic infection has been reported in
domestic cats (see References: Leschnik 2007). FAO recommends that avian
influenza in cats should be closely monitored (see References: FAO: 2007).
H5N1 in humans: epidemiologic features
WHO has officially recognized more than 300 human cases of H5N1 influenza;
cases have been reported from Azerbaijan, Cambodia, China, Djibouti, Egypt,
Indonesia, Iraq, Lao People’s Democratic Republic, Nigeria, Thailand,
Turkey, and Vietnam (see References: WHO: Cumulative number of confirmed
human cases of avian influenza A [H5N1]; WHO: Situation updates).
The case fatality rate is higher than 50 per cent overall and higher than
70 per cent presently in Indonesia, according to WHO numbers. An
epidemiologic report on 256 confirmed H5N1 influenza cases published by WHO
in February 2007 demonstrated that the median age of cases was 18 years and
that 89 per cent of infections occurred in persons under 40 years of age
(see References: WHO: Update: Epidemiology of WHO-confirmed human cases of
avian A[H5N1] infection, 25 Nov 2003 - 24 Nov 2006). The overall case
fatality rate for this period was 60 per cent and the median number of days
from symptom onset to death was 9 days. Most recognized human cases have
involved direct contact with poultry (see References: WHO Writing Committee
of the WHO Consultation on Human Influenza A/H5 2005).
Types of exposures that have been identified to date include:
•   Slaughtering, plucking and preparing diseased birds
•   Handling fighting cocks
•   Playing with poultry (particularly asymptomatic ducks)
•   Consumption of duck blood and possibly undercooked poultry

Low perceived risk and high population exposures to live chickens appear to
be factors that are contributing to the spread of H5N1 from infected birds
to humans (see References: Fielding 2005). For example, a survey of
households in an area of rural Thailand affected by avian influenza found
that 74 per cent of households surveyed owned live poultry (see References:
Olsen 2005: Poultry-handling practices during avian influenza outbreak,
A recently published report of a case-control study from Vietnam found that
the following risk factors were independently associated with H5N1
infection (see References: Dinh 2006):
•   Preparing sick or dead poultry for consumption in the 7 days before
illness onset
•   Having sick or dead poultry in the household in the 7 days before illness
•   Lack of an indoor water source.

Another recent case report suggests that food markets with live birds may
be a source of exposure for avian influenza (see References: Wang 2006).
Following recognition of a case of avian influenza in a rural village in
southern Cambodia in 2005, investigators conducted a retrospective survey
of poultry deaths and a seroepidemiologic survey of villagers (see
References: Vong 2006). Of 194 households in the area, interviews were
completed for 163; 155 of these households raised chickens or ducks and 42
households were likely to have had an outbreak of avian influenza between
January and March 2005 in their poultry (based on high rates of illness and
mortality among chickens). Serologic testing of villagers approximately 2
months after outbreaks in poultry did not demonstrate any recent H5N1
infections, despite close contact with birds likely to have been infected
with H5N1.
These findings illustrate the following: (1) H5N1 was not easily
transmitted from birds to humans and (2) asymptomatic or mildly symptomatic
human infections did not occur. A survey of 257 poultry workers in Italy
regarding knowledge, attitudes, and practices around avian influenza found
that workers in that area had a relatively low perceived risk of avian
influenza and did not routinely practice biosecurity measures (such as
wearing protective equipment and handwashing) (see References: Abbate 2006).
The first report of H5N1 disease in humans contracted through exposure to
wild birds occurred in the spring of 2006 (see References: Gilsdorf 2006).
The discovery was made in a cluster of human cases in Azerbaijan; family
members denied any contact with ill domestic poultry, but many wild swans
had died in the area and were thought to have played a role.
In August 2006, CDC released a set of guidelines for conducting
surveillance on dead birds (see References: CDC: Interim guidance for
states conducting avian mortality surveillance for West Nile virus (WNV)
and/or highly pathogenic H5N1 avian influenza virus). To date, sustained
person-to-person transmission has not been recognized, although probable
person-to-person spread was identified in Thailand involving transmission
from an ill child to her mother and aunt (see References: Ungchusak 2005)
and several other familial clusters have been recognized (see References:
Olsen 2005: Family clustering of avian influenza A [H5N1]).
In May 2006, WHO reported an H5N1 influenza cluster in Indonesia involving
7 cases of person-to-person transmission; one of the cases involved 2
generations of transmission (see References: WHO: Avian influenza:
Situation in Indonesia: Update 14 and see 24 May 2006,
CIDRAP News story).
An Indonesian official recently put the number of clusters in that country
at 10, all involving cases in blood relatives (see 12 Jan 2007,
CIDRAP News story).
Inefficient transmission of current H5N1 strains may be related to lack of
appropriate avian virus cell receptors in the upper respiratory tracts of
humans and the inability of H5N1 strains to recognize human cell receptors
(see References: Shinya 2006). A mutation allowing H5N1 avian influenza
virus to recognize human cell receptors could enhance person-to-person
transmission owing to the potential for greater viral replication in the
upper respiratory tract. Intensified surveillance in northern Vietnam
suggests that the local strains are adapting to humans. These efforts have
identified less severe cases, more infections in older adults, and a few
family clusters that suggest person-to-person spread (see References: WHO
Writing Committee of the WHO Consultation on Human Influenza A/H5 2005).
The entire text is supplemented by comprehensive referencing of original
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Anti_Illuminati November 06, 2009, 11:15:39 PM

Live, Attenuated Influenza A H5N1 Candidate Vaccines Provide Broad Cross-Protection in Mice and Ferrets

by: Amorsolo L. Suguitan, Josephine Mcauliffe, Kimberly L. Mills, Hong Jin, Greg Duke, Bin Lu, Catherine J. Luke, Brian Murphy, David E. Swayne, George Kemble, Kanta Subbarao
PLoS Medicine, Vol. 3, No. 9. (September 2006)


Recent outbreaks of highly pathogenic influenza A H5N1 viruses in humans and avian species that began in Asia and have spread to other continents underscore an urgent need to develop vaccines that would protect the human population in the event of a pandemic.

Methods and Findings
Live, attenuated candidate vaccines possessing genes encoding a modified H5 hemagglutinin (HA) and a wild-type (wt) N1 neuraminidase from influenza A H5N1 viruses isolated in Hong Kong and Vietnam in 1997, 2003, and 2004, and remaining gene segments derived from the cold-adapted (ca) influenza A vaccine donor strain, influenza A/Ann Arbor/6/60 ca (H2N2), were generated by reverse genetics.

The H5N1 ca vaccine viruses required trypsin for efficient growth in vitro, as predicted by the modification engineered in the gene encoding the HA, and possessed the temperature-sensitive and attenuation phenotypes specified by the internal protein genes of the ca vaccine donor strain. More importantly, the candidate vaccines were immunogenic in mice. Four weeks after receiving a single dose of 106 50% tissue culture infectious doses of intranasally administered vaccines, mice were fully protected from lethality following challenge with homologous and antigenically distinct heterologous wt H5N1 viruses from different genetic sublineages (clades 1, 2, and 3) that were isolated in Asia between 1997 and 2005.

Four weeks after receiving two doses of the vaccines, mice and ferrets were fully protected against pulmonary replication of homologous and heterologous wt H5N1 viruses.

The promising findings in these preclinical studies of safety, immunogenicity, and efficacy of the H5N1 ca vaccines against antigenically diverse H5N1 vaccines provide support for their careful evaluation in Phase 1 clinical trials in humans.
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Anti_Illuminati November 10, 2009, 03:06:12 PM,9171,1101980223-138630,00.html

The Flu Hunters
By Erik Larson/Hong Kong Sunday, Jun. 24, 2001

It was a subtle warp in an otherwise routine day. Dr. Wilina Lim, chief virologist with the Hong Kong Department of Health, was sorting through the usual load of blood and tissue specimens sent to her laboratory from nearby hospitals, typically about 80 a day. On this particular day--Tuesday, May 20, 1997--one specimen came from Queen Elizabeth Hospital in Kowloon, at the far side of Victoria Harbor, where a three-year-old boy had been admitted with what turned out to be a fatal respiratory illness. Her lab quickly determined that the infectious agent was some type of Influenza A, one of two broad classes of flu virus that commonly affect humans. To identify the specific strain or subtype, the lab tested the sample, using reagents distributed by the World Health Organization. The test kits triggered no response.

Lim was intrigued but not terribly concerned. While she did not often receive flu viruses that resisted identification, it did happen. She retested the virus and again got no reaction. A month later, she forwarded samples to the Centers for Disease Control and Prevention in Atlanta and to England's Mill Hill, two laboratories in the top tier of a quiet but elaborate global surveillance network that tracks changes in the world's flu viruses. Almost as an afterthought, Lim sent a sample to Jan De Jong, a virologist at the Dutch National Institute of Health and the Environment who liked to collect unusual strains of influenza. She had never met De Jong, but over the years they had developed a rapport.

For more than a month, she heard nothing. Then suddenly, on Friday, Aug. 8, De Jong called. He was coming to Hong Kong. He had booked a flight that day. He would arrive Sunday. It seemed, at first, just a friendly visit--a chance, at last, to meet face to face.

Lim picked him up at the Kowloon Ramada on Monday morning. As she drove back to her laboratory, high in Hong Kong's craggy western hills, De Jong turned to her and asked mildly, "Do you have any idea what virus you sent me?"


By now most of the world has heard of the "bird flu" that emerged in Hong Kong last year, infecting 18 people and killing six. One patient, a young woman, remains on a ventilator under intensive care. Although no new cases have been discovered since Dec. 28, virologists consider the emergence of this new virus one of the most significant and worrisome medical events of the day. And they don't think the danger has passed. In fact, the critical period could just now be arriving in Hong Kong. This is the start of the traditional flu season, when the new virus could, in theory, combine with ordinary human strains to create a supervirus that is both lethal and highly contagious.

While the outbreak highlighted the success of the surveillance network, it also showed how dangerously mutable influenza viruses can be and that, in their most sinister forms, they can be as deadly as any other disease known to man, more akin to Ebola than to the fevers and aches most people associate with flu. Virologists say the decision to kill all the chickens in Hong Kong--widely derided at the time--was in fact the smartest thing that could be done and that it might have prevented a more widespread disaster. "The question is," says Robert Webster, chairman of the virology department at St. Jude Children's Research Hospital in Memphis, Tenn., and a key actor in the quiet drama played out in Hong Kong, "did they close the stable door before or after the horses had gone?"

The CDC grabbed most of the headlines with its usual Ghostbusters aplomb, and even dispatched a public relations officer to accompany the agency's team of epidemiologists. But at least three investigations coalesced in Hong Kong. Only by following all three does the true significance of the outbreak become clear. Taken together, these threads weave a story that begins 80 years ago and winds forward through venues as varied as a high-security lab in Ames, Iowa, the ancient tissue collections of the Armed Forces Institute of Pathology in Washington and a frozen mass grave on Alaska's Seward Peninsula.

The Hong Kong Incident, as Webster calls it, arrived with cinematic timing--an almost supernatural confluence of event and inquiry. It occurred amid heightened sensitivity to the dangers of newly emerging viruses and just as several teams of researchers were closing in on the mysterious 1918 "Spanish flu," which killed more than 20 million people. At the same time, it turns out, public-health officials were quietly intensifying plans for the next great global epidemic, or pandemic.

While the rest of the world was wringing its hands over the remote threat from such exotics as Ebola and hantavirus, the health officials were busy staring down a far more likely global disaster and produced a closely held Pandemic Planning Document. In the course of their meetings, the planners are said to have wrestled with such issues as what to do if the President dies and how to deal with masses of dead or severely ill citizens, considerations reminiscent of civil-defense planning for nuclear war. The planners are so certain that another worldwide epidemic will occur that they refer to the present as the "interpandemic period."

The full story of the Hong Kong Incident begins in 1918 with the most lethal epidemic in human history, one that eclipsed even the medieval Black Death. "It's why we do what we do every year," says Roland A. Levandowski, the Food and Drug Administration's chief flu expert and a member of the pandemic planning group. "This experience in Hong Kong, even if it doesn't go anywhere, is a reminder that these things can happen."


The pandemic of 1918 remains a mystery. It began with a relatively mild initial assault on March 4, when the first reported case occurred at Camp Funston, Kans. Within four months, the virus had traversed the globe. The flu sickened millions but killed relatively few, and in the tumult of World War I, the first wave seemed pretty mundane.

No one knew it at the time, of course, but flu viruses are notoriously unstable-- "genetically labile," as one researcher puts it. Set one flu virus beside another, and the two may trade genes, a process called reassortment. If this reassortment produces a virus that closely resembles one of its parents, it is said to have undergone antigenic drift. On rare occasions, this scrambling can be dramatic. The virus becomes a kind of Frankenstein virus so different from existing strains that the human population has no immunity to it.

In August 1918, the mild virus apparently reassorted into something positively deadly. Outbreaks caused by the new variant exploded almost simultaneously in three far-flung locations: France, Sierra Leone and Boston. The flu struck with a ferocity that shocked doctors, who feared this strange new pathogen might be an airborne version of the Black Death. Patients died awash in blood and gore, literally drowning as fluid filled their lungs.

The virus rocketed to the farthest points of the globe. From September 1918 through March 1919, it killed 33,387 people in New York City, just over 1% of the city's population. In some Alaskan villages, the death toll topped 50%; in one, Teller Mission (now Brevig Mission), 85% were dead within a week.

One of the great mysteries of 1918 centers on who was killed by the virus. Even ordinary flu will cause deaths among the very young, the very old and people with a weakened immune system. The 1918 virus did kill within these groups, but it seemed to have a special passion for the young and hardy, ages 25 to 34, those typically most able to weather the flu.

Rumors flew of strange influenza-like diseases affecting animals, even moose, according to the pandemic's chronicler, Alfred W. Crosby Jr. One rumor turned out to be true--disturbingly so for anyone familiar with the subsequent history of influenza research and the recent Hong Kong outbreak. Farmers in 1918 discovered that something was making their pigs very sick, with high fevers and bad coughs. No such pig flu had ever been noticed before 1918, but every fall thereafter an influenza-like illness attacked the nation's hog population. In 1928 a researcher from the Rockefeller Institute, Richard E. Shope, went to Iowa to investigate the phenomenon, and in 1930 he became the first scientist to isolate an influenza virus. Copies of it are stored today in laboratories around the world.

The 1918 strain of influenza persisted into the '20s, then disappeared, or lost its virulence and faded into the great jigsaw of constantly reassorting viruses. Until lately, the epidemic had almost disappeared from our collective memory as well, prompting Crosby to title his history The Forgotten Epidemic. Among flu experts, however, its mysteries are still current and utterly significant. It has always stood as a vivid warning of what the next pandemic could be like. What made the virus so lethal? Why was it able to kill so quickly? And where in nature did it originate?

Last year flu researchers found themselves asking the same questions once again, but this time because of the strange events in Hong Kong.


It was March of 1997 when the chickens began to die--6,800 on three farms in Hong Kong's rural New Territories. Because poultry is a vital part of Hong Kong's diet, agricultural authorities got concerned and quickly consulted Kennedy Shortridge, a microbiologist at the University of Hong Kong. He in turn contacted his friend and fellow flu specialist Robert Webster of St. Jude. For decades both men had studied influenza viruses in chickens and other birds in the belief that these viruses were more than just an agricultural problem and might hold the key to the origins of human influenza, possibly even the virus of 1918.

Shortridge and Webster immediately recognized the gravity of the chicken-flu outbreak in Hong Kong, at least for the region's chicken industry. They knew that while avian influenza did not ordinarily make its host sick, a benign virus could reassort to produce a pathogen of almost inconceivable lethality. Webster's Memphis lab had observed such a transformation in the wild on two occasions, the first in April 1983, when a relatively mild influenza struck chickens on the vast chicken farms of Pennsylvania. The birds got visibly sick, some died and egg production fell, but overall the outbreak remained only a vexing economic problem.

By October, the virus had changed. Before, it attacked the respiratory and intestinal tracts of chickens; now, suddenly, it assaulted every tissue in the chickens, including the brain. It caused all their blood vessels to leak and killed them within days, turning the birds, as one researcher put it, into "bloody Jell-O." Federal inspectors arriving at Pennsylvania farms found themselves walking through factory-size chicken coops struck eerily silent, with thousands of dead or hemorrhaging chickens at their feet. The U.S. Department of Agriculture ordered the extermination of 20 million chickens in Pennsylvania, more than 10 times the number that would be killed in the Hong Kong chicken slaughter.

Webster assigned a young scientist, Yoshihiro Kawaoka, to try to figure out how the virus transformed itself into such a "hot" pathogen. Kawaoka, now a professor of virology at the University of Wisconsin, Madison, compared the genetic structure of viruses from the first and second waves and found only a single, extremely subtle change in the H gene. The two viruses differed by just one nucleotide--one of 1,700 nucleotides that made up the gene.

Last year, on two of the three farms stricken in Hong Kong, mortality was 100%. The scientists knew the virus had a variation of the H gene known as H5--one that is notoriously lethal to chickens. Shortridge did briefly wonder if the virus might eventually cause problems for humans. In an earlier study, conducted with great discretion, his lab had found that residents of rural Hong Kong had antibodies to all the known bird-flu viruses. What that suggested, says Shortridge, was that "any virus could cross the species barrier to humans. But whether it could set up an infection, be established as an infection and maintained as an infection is, of course, another matter."

Shortridge, in Hong Kong, asked Webster, in Memphis, if he could help him arrange to ship a sample of the deadly virus for in-depth analysis to the U.S. Department of Agriculture's high-security laboratory in Ames, Iowa. When the package arrived, it was sent to a P3+ containment laboratory--one notch below the P4 level required for studies of Ebola virus--where Dennis Senne inoculated the virus into chicken eggs and chickens to gauge its pathogenicity. It killed 10 out of 10 chickens; each died within one or two days.

Senne then subjected the virus to detailed genetic analysis, a process known as gene sequencing. On the H gene at a point called the cleavage site, he found a telltale mutation, the same kind of mutation found in other highly pathogenic avian viruses. Senne shipped his findings and samples of the virus to Webster, who analyzed its viral heritage. The virus, he discovered, had regions that were identical to portions of the avian virus that struck Pennsylvania in 1983.

The outbreak in Hong Kong was quickly contained. All birds on the three farms were destroyed. And that's where Webster and Shortridge left it. "At that point," Webster remembers, "it was merely interesting."


In March, even as the chickens were dying, a molecular pathologist at the Armed Forces Institute of Pathology in Washington, Dr. Jeffery Taubenberger, startled the flu research community with a paper in the prestigious journal Science in which his team claimed to have at least partly penetrated the fog surrounding the 1918 pandemic. The coincidence was striking: just as a new virus was emerging in Hong Kong, here was fresh news about the mother of all epidemics.

Taubenberger's work began not out of some great passion to plumb the mysteries of 1918 but rather a desire to showcase two of the Pathology Institute's crown jewels: its vast collection of tissue specimens gathered over the past century, and its new technique for extracting RNA from biological materials fixed in Formalin and paraffin. Even he, however, wondered if the institute's tissue repository, "the annex," would be able to locate such old specimens. He had never seen the place and pictured it as a forlorn vault like the vast warehouse in the closing scene of Raiders of the Lost Ark. Taubenberger and colleague Ann Reid put in a request to the annex for tissue samples of three dozen soldiers who had died in the 1918 pandemic. They then settled in for what they assumed would be a long wait.

They assumed wrong. The repository, housed in a nondescript building 10 minutes away in Forest Glen, Md., is not the gloomy storehouse they imagined. A few seconds after receiving Taubenberger's request, the annex's robotic retrievers had located the laboratory slides associated with his cases, rising on quiet greased chains to retrieve them from the upper reaches of a 10-ft.-tall, room-length revolving carousel. A few days later, a collection of small brown lunch bags turned up at Taubenberger's office, each marked with a case number, each containing flecks of tissue taken from a young soldier killed by the flu nearly a century earlier, by doctors struggling to cope with a lethal epidemic they did not understand. For Taubenberger and Reid, it was a strangely haunting moment.

The hard work was just beginning for Reid. She would spend the next year searching through the samples for a snip of 1918 RNA.


As Wilina Lim drove back to her laboratory with Jan De Jong, the Dutch researcher, she considered his question about the nature of the virus she had sent him. Clearly he already knew what it was. She thought a moment, then guessed the virus was probably an H3, common in humans, that had changed sufficiently to evade detection.

"No," De Jong told her. "It was H5."

Lim was startled. "I'm not a vet," she says. "I don't know much about influenza in animals." But she had never heard of H5 infecting humans. For it to do so now was surprising. Even impossible.

And suddenly she understood why De Jong had felt it necessary to come in person to Hong Kong, why he had waited until now to tell her about the virus. He suspected that the H5 had not really come from human patients but was the result of laboratory contamination. Everyone knew that her lab was situated close to Shortridge's and that Shortridge worked with avian viruses. Moreover, this was Hong Kong, where poultry stalls with live chickens could be found in the same neighborhoods as five-star hotels. "I think he came to Hong Kong to have a look-see if it was a sloppy laboratory," says Lim. She knew his concern was justified, but still it offended her. She is known for her buoyancy, but at this moment her expression hardened. "I knew it was not a contaminant," she says, "because I know my lab."

And soon De Jong was also convinced. That night he spoke with Albert Osterhaus, chairman of the virology department at Erasmus University in Rotterdam, where virologist Eric Claas had analyzed the suspect virus using a panel of reagents derived from flu strains isolated and maintained by Webster. Claas had first determined that the virus was H5N1, well before the CDC and Mill Hill. At the outset even he did not believe it. An H5 infection in humans was unheard of. He too assumed the H5 was a contaminant.

Meanwhile Osterhaus had called Webster in Memphis to learn more about H5. Only then, in that phone call, did the human-flu research community at last learn of the earlier outbreak of chicken flu on the three Hong Kong farms; and only then did Webster and Shortridge learn of the first human case--even though Shortridge's laboratory and Lim's are housed in adjacent buildings.

Webster already had the virus in his collection, its genetic structure detailed, its heritage mapped. He recalls, with obvious delight, how he told Osterhaus, "Abe, I have the precursor of this virus in my laboratory."

For Webster, it was an exciting moment. "The situation in Hong Kong is what I've been predicting throughout my career," he says. For years, he contends, people have dismissed avian flu "as a problem of chickens--who cares?" He revels in his newfound credibility. "Finally," he says, laughing, "at the end of my career, the chickens have come home to roost."

He concedes, however, that he was startled when Osterhaus told him about the three-year-old boy who had died on May 21, the day after Lim received his specimen. Webster also wondered whether the H5 was merely a contaminant. Osterhaus assured him it was not. After the call, Webster taped a note to the wall over his desk: H5 IN A CHILD!


Like Webster, virologists around the world were galvanized. The CDC, alerted by Claas, quickly tested its own copy of Lim's virus and confirmed the finding. In San Francisco, Dr. Keiji Fukuda, chief epidemiologist for the CDC's influenza section, was doing a clinical rotation at Mount Zion Hospital when he received an urgent call from the agency's head of surveillance. "Whenever you get a call like that," he says, "you know it's probably not great news." Shortridge was vacationing in England when his phone went wild. "The first thing that crossed my mind was, 'Is this the start of a new pandemic?' " he recalls.

To anyone who knew influenza, the news instantly raised the specter of 1918. Or worse, as this was a purely avian virus against which most humans would have no defense. The world, moreover, was far more densely populated, and high-speed travel now linked all the major cities. In 1918, when transportation was still painfully slow, the pandemic circled the globe in a matter of months. Traveling by jet, a new killer virus could reach Tokyo in three hours and New York City within a day.

The fact that the new virus did not seem readily transmittable from person to person was a consolation, but flu experts know that influenza viruses are utterly unpredictable. In Hong Kong the big question was this: Would the H5 reassort with a common human strain to produce a new virus that was as lethal as H5 but could be passed along by a human sneeze? Or would this new H5 virus, through repeated exposure, find some other way to adapt to human hosts? "That's an interesting point," says Shortridge, "because it raises questions about the 1918 pandemic. Did a similar sort of thing happen?"


Back in Washington, Taubenberger and Reid had decided to concentrate on the seven cases in which the victim had died most quickly, figuring that these specimens would be most likely to retain the genetic remains of the virus. They found plenty of RNA, but none of it looked like flu--until, after a full year's work, they came to Private Roscoe Vaughn.

Vaughn was a 21-year-old soldier at Camp Jackson, S.C., who reported for sick call on Sept. 19, 1918, at the peak of the pandemic. He complained of chills, fever, headache and a bad cough. He had trouble breathing. A week later, at 6:30 a.m., he died. At 2 p.m., his body was autopsied, and specimens were extracted, preserved and sent to Washington.

Using an array of powerful if arcane gene-hunting tools, Taubenberger and Reid slowly picked their way through the shattered genetic landscape of Private Vaughn's cells. This time they got lucky. They found small pieces of flulike RNA. Their subsequent analysis showed that the virus was an H1N1 influenza unlike any flu virus identified during the past 80 years. The closest known strain was Swine Iowa 30--the pig flu isolated by Richard Shope in 1930 and kept alive at various culture repositories ever since. Their findings suggest that the 1918 virus came to people from pigs, not from birds--although Taubenberger cites studies by Webster and others indicating that human viruses and the pig flu of the 1930s may share a common avian ancestor. This suggests that sometime before 1918, a bird virus could have entered the mammalian population and, through reassortment, produced the pathogenic flu virus known to man.


The CDC's Fukuda arrived in Hong Kong on Wednesday, Aug. 20. The next day he and a team of CDC investigators joined an intensive investigation already being conducted by the Hong Kong Department of Health. Working with health-department officers, Fukuda and his colleagues conducted scores of interviews and collected hundreds of blood samples, trying to figure out how the first victim, the three-year-old boy, could have contracted a virus that infects only birds.

The CDC took a hard look at the boy's preschool, in particular a corner of his classroom set aside as a kind of nature corner, with live chicks and ducklings. Fukuda knew that the birds had died before the boy got sick, but no one knew what killed them. The team swabbed the classroom floor to try to capture some of the virus, but found none. Although press reports suggested a close tie between the death of the classroom birds and the boy's illness, Fukuda says the source of the boy's infection is by no means certain. "It was unclear then," he says. "It is unclear now."

The CDC's investigation of the boy's illness lasted 2 1/2 weeks. By the time Fukuda left Hong Kong, his team had collected 2,000 blood samples. Antibodies indicating previous exposure to H5N1 were found in only nine samples, including one of the boy's classmates and one of his doctors. None of the nine recalled being ill. The fact that so few showed signs of exposure was concrete evidence that the virus was not particularly contagious.

For the moment, there appeared little reason to fear that this first case, however tragic, represented the start of a pandemic. Says Fukuda: "I left thinking, 'You know, this is probably some odd, sporadic thing.'"

He expected no more cases.


In another odd coincidence, that same August, as Fukuda investigated the new virus in Hong Kong, the quest to understand the 1918 epidemic suddenly gained momentum, with help from a surprising quarter. Out of the blue, Taubenberger got a letter from a retired San Francisco pathologist, Johan Hultin, who had read Taubenberger's paper in Science and saw at last an opportunity for which he had been waiting for nearly a half-century.

In 1951 Hultin took part in an expedition to Alaska to try to extract live virus from long-frozen victims of the 1918 flu in what is now Brevig Mission, Alaska. Now he was ready to try again. He knew from hard experience that no live virus had survived under the permafrost. But Taubenberger's paper convinced him that technology had advanced to the point where even a dead virus could be of immense value. The moment he saw the Science paper, he told himself, "There. This is it."

Hultin asked Taubenberger whether he would accept and analyze samples of lung tissue from frozen graves, if he, Hultin, went to Alaska to get them. "When are you planning to leave?" Taubenberger asked. He knew firsthand that such ventures take a lot of advance planning. "I can't go this week," Hultin told him. "But I can go next week." Taubenberger got really quiet. "I don't know what was going through his mind," Hultin says, chuckling. "He probably thought I was some kind of a nut."

Two weeks later, Hultin was on his way--one 73-year-old man with a sleeping bag, a carry-on bag and two duffels full of equipment. He traveled solo and avoided publicity so as not to raise too much fuss among Brevig's villagers. By the afternoon of Aug. 20, he and a local crew had begun digging, and they eventually produced a trench 6 ft. wide, 27 ft. long and 7 ft. deep. Hultin came across several bare skeletons before he hit pay dirt: the well-preserved body of a 30-year-old woman so obese that her fat had insulated her organs from the effects of decades of frost and thaw. He took both lungs, sliced them into thin strips and carefully packed them for shipment. Hultin named the body "Lucy," a nod to the prehistoric Lucy who shed so much light on human origins.

Hultin expected to wait months to hear of any results, but Taubenberger called within a few weeks. He had found fragments of the 1918 virus in Hultin's Lucy. Taubenberger and Reid had meanwhile recovered yet another sample of 1918 virus from tissues in the Armed Forces annex. Taken together, the three samples put to rest any doubt that Taubenberger's lab had indeed found and sequenced key portions of the original Spanish-flu virus.

Hultin says he was struck by the uncanny timing of his journey, which took place just as a strange virus with great pandemic potential was emerging in Hong Kong. "I was very apprehensive," he says. "I was waiting for it to come--and it didn't." But another pandemic, he believes, is inevitable. He has given his wife instructions on what to do to survive it: retreat to their mountain cabin until the onslaught passes. It was a tactic, he knows, that was successfully used in 1918 by a village just 30 miles from Brevig. Its elders, after learning of the advancing plague, stationed armed guards at the village perimeter with orders to shoot anyone who tried to enter. The village survived unscathed.


Hong Kong, in the meantime, had begun to relax. From August into November, nothing happened. No new cases appeared. In postmortems on the first case, researchers congratulated themselves on how well the global flu-surveillance system had worked. Some even suggested that it worked too well, that the avian flu had been discovered only because the surveillance network was looking for such events and that isolated bird-to-human infections had probably happened before and gone undetected.

On Nov. 8, Lim's virology lab got its usual load of new specimens to analyze, including one from a two-year-old boy admitted the day before to Queen Mary Hospital. Her lab applied the ordinary WHO reagents for H3 and H1, but just as in May, got no reaction. This time Lim tried an H5 reagent supplied by the CDC. And got a positive reading.

By now, however, the patient had already been discharged, well on his way to full recovery. In fact, he had been only mildly ill and was admitted because of a heart condition that made him vulnerable to even routine infections.

"So now I think, 'This cannot be,'" says Lim. Perhaps it was contamination, after all; maybe this H5 reading had been caused by the presence of the H5 she had grown and tested in May. She asked the hospital to send over anything that remained of the material originally swabbed from the boy. This too tested positive for H5. "Now I'm worried," she says, "because after six months it came out again."

Webster was in Memphis driving home from a Saturday at work when his wife told him he had received a call from the CDC. He called back, waited, called again, and this time got the news: "The virus is moving."


On Dec. 1, Queen Elizabeth Hospital sent Lim a specimen from a 54-year-old male who had developed a fever and a cough and soon had to be admitted, apparently suffering from pneumonia. Four days later, Lim's lab succeeded in growing a virus extracted from his specimens. The next day, the patient died. Lim tested the virus with her H5 reagents. Again, a positive.

Lim knew that she had another specimen in her lab, taken from a 13-year-old girl admitted to Prince of Wales Hospital so sick that she had been placed on a respirator. The hospital had identified the underlying virus as Influenza A but wanted Lim to determine the subtype. Lim asked her lab technicians to come in early the next morning, Saturday, Dec. 6, to test specimens from the two patients. Both again reacted to the H5 reagents.

By then the CDC's Fukuda was already in the air, aware only of the initial two cases--not Lim's most recent discoveries. That weekend Lim's daughter complained of a sore throat. Instantly the dispassionate virologist became a frightened mother. She barred her daughter from all sports and canceled her piano lessons.

As his plane crossed the Pacific, Fukuda consoled himself with the fact that in six months only two cases of H5 flu had occurred. Upon his arrival, a medical officer with the Hong Kong Department of Health greeted him warmly, then gently told him of the latest discoveries. "The good news," the officer said, "is we will have a nice dinner. The bad news: there are two more cases."

This brought the total to four. Two patients had died. One was on a respirator. Fukuda, a member of the pandemic planning committee, suddenly had a glimpse of what it might be like to confront an explosive outbreak. It is one thing to plan rationally, he says. "It's another thing all of a sudden to be struck with a sense that, my God, what will happen if there are a thousand cases like this? What will happen to all of those people? How will hospitals cope? How will any of us cope?"

In short order, more cases began turning up throughout Hong Kong. On Dec. 4, a 24-year-old woman developed a fever, sore throat and cough, and complained of dizziness. Five days later, she was in the intensive-care unit on a respirator with a confirmed case of H5 influenza. On Dec. 7, a five year-old girl began vomiting and developed other flu symptoms. H5 again. On Dec. 12, another child, a cousin of the five-year-old, came down with a fever and was hospitalized with H5. And a new outbreak of H5 had turned up on a fourth chicken farm in the New Territories.

In Fukuda's war room, Room 58 of the health department's downtown headquarters, a large whiteboard listed all the cases and tracked their medical progress. A big downward arrow meant death. With new urgency, Fukuda and the CDC hunted the sources of infection, collecting 3,000 blood samples and helping question some 2,500 people.


To Webster and Shortridge, Hong Kong's many outdoor markets held the key to why the confirmed cases of H5 were spread in such haphazard fashion throughout Hong Kong. In some cases, the CDC team and health-department investigators were unable to prove direct contact with poultry, which suggested that some of the victims caught the virus through contact so casual they simply weren't aware of it. Says Shortridge: "It suggested to me there was a hell of a lot of virus in the environment that we weren't aware of."

Webster and Shortridge quickly arranged an ad hoc task force to begin testing poultry in the city's "wet" markets, so named because retailers use water to clean their stalls and adjacent sidewalks. The group began its probe on Dec. 22 and worked 18 hours a day right through Dec. 28, the day Hong Kong authorities began their territory-wide slaughter. The research showed that 10% of chickens in the markets carried the virus. Ducks and geese in the markets carried it too--especially worrisome, given their ability to carry infections without outward sign of illness. In the markets, all poultry--ducks, geese, chickens--was killed. The slaughter, according to Shortridge and Webster, removed a substantial reservoir of H5 virus from contact with people.

Then suddenly, almost as soon as it started, the second outbreak seemed to be over. The last case occurred on Dec. 28, the day the slaughter began. By late January, Fukuda's whiteboard in Room 58 showed 18 confirmed cases, with six downward arrows.


A killer had come and gone, raising new mysteries even as old mysteries from 1918 were being solved. What allowed this avian virus to cross the species barrier and set up killing infections in man? Why did it strike the young and hardy with the most ferocity--just as the 1918 virus had? And, most important, has the virus really ceased to be a threat, or is it circulating more quietly, primed for a "reassortment event" that will set off the next global disaster?

So far, the new virus has shown no evidence of reassortment. The fact that the outbreak happened in December, before Hong Kong's regular flu season, reduced opportunities for reassortment, as did the prompt slaughter of the chickens. But the flu season is coming. It will peak in late February and early March, with a second peak this summer. What researchers fear most is that someone infected with a common flu strain will also become infected with H5, and thus become an inadvertent mixing chamber for the production of a wholly new virus.

Webster and Shortridge are convinced that the avian virus is still circulating in the environment. "I don't think we're out of the woods yet," says Shortridge. Fukuda agrees: "You would be a fool to predict what the virus is going to do next. I'm equally prepared for this thing to disappear as I am to hear one day when I walk into the office, 'Oh, did you hear? There's another 10 cases--or 100 cases.'"

It would be easy to dismiss the Hong Kong Incident as just a one-time quirk of blood and protein. But the U.S.'s leading flu experts seem unwilling to do so. This became particularly apparent at the annual meeting of the FDA Vaccine Advisory Panel, convened two weeks ago in Bethesda, Md., to decide what flu strains should be targeted for next year's flu vaccine. Ordinarily these meetings are routine, if not downright boring. But this year the committee devoted half the day to the Hong Kong outbreak.

For Webster, it was a striking moment--the first time he had ever been invited to the meeting, a point he made clear in the opening moments of his talk. Equally striking, no one on the panel tried to minimize the potential danger of the new avian virus. Far from it. In a vote the FDA had not even requested, the committee unanimously agreed to move ahead to develop a vaccine against H5, even take it through clinical trials.

Shortly before the vote, Webster was asked his opinion. He believes the Hong Kong Incident may have given the world early warning of more H5 outbreaks to come. "We have a window of opportunity," he told the assembled scientists. "Let's do it now."
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-Vaccine=rev genetics w/PROMIS
: Anti_Illuminati November 10, 2009, 03:40:49 PM,8599,1114634,00.html

Catastrophic 1918 Pandemic Was Also A Bird Flu
By Michael Lemonick Thursday, Oct. 06, 2005

1918: Flu victims crowd into an emergency hospital in Kansas

For two years now, public health experts have been nervously monitoring the progress of a virulent strain of influenza known as H5N1, which has killed 140 million birds, mostly in Asia. Humans catch it too—100 or so have been hospitalized with the illness worldwide, and about 60 have died—but since this flu doesn't pass directly from one person to another, it isn't a serious threat so far. If it mutates, though, to allow easy human-to-human transmission, scientists fear it could rival the legendary Spanish flu pandemic of 1918 and 1919, which ravaged the planet, killing more than 50 million people.

A series of papers published this week in the journals Science and Nature suggest that such a mutation is all too plausible. Working from snippets of tissue from victims of that long-ago plague—one from an Inuit woman buried in permanently frozen soil in Alaska, two others from autopsy samples taken from American soldiers who died in the Northeast—scientists from the Armed Forces Institute of Pathology, the Centers for Disease Control and other institutions determined that the lethal Spanish flu was itself a bird flu that evolved to infect humans directly.

None of the tissue samples contained an intact virus, but the researchers used the fragments they found to recreate the lethal virus, which they tested in mice and on human lung cells to confirm its virulence. They discovered that the 1918 bug was different in one crucial way from the viruses responsible for the flu pandemics of 1957 and 1968, better known as the Asian and the Hong Kong pandemics. (A pandemic is a worldwide epidemic.) Those were human influenza viruses that had incorporated a few bird flu genes, but the 1918 virus was a bird flu that changed to permit more efficient human-to-human transmission. It wasn't that many changes, either. Dr. Jeffery Taubenberger, one of the investigators, estimates that it took only about 25 mutations to cause that change—not a very large number, considering that influenza viruses mutate relatively easily. (That's why at least one new strain appears nearly every year).

It isn't yet clear precisely which mutations are key to turning a lethal bird flu into a worldwide human health crisis. And it's by no means certain that H5N1 will make that deadly leap. But sooner or later, experts say, it will happen. That's why 65 nations are meeting today and tomorrow in Washington to try and figure out how to respond when it does.

The Guardian, Thursday 6 October 2005
Ian Sample, science correspondent

Security fears as flu virus that killed 50 million is recreated

Scientists have recreated the 1918 Spanish flu virus, one of the deadliest ever to emerge, to the alarm of many researchers who fear it presents a serious security risk.

Undisclosed quantities of the virus are being held in a high-security government laboratory in Atlanta, Georgia, after a nine-year effort to rebuild the agent that swept the globe in record time and claimed the lives of an estimated 50 million people.

The genetic sequence is also being made available to scientists online, a move which some fear adds a further risk of the virus being created in other labs.

The recreation was carried out in an attempt to understand what made the 1918 outbreak so devastating. Reporting in the journal Science, a team lead by Dr Jeffery Taubenberger at the Armed Forces Institute of Pathology in Maryland shows that the recreated virus is extremely effective. When injected into mice, it quickly took hold and they started to lose weight rapidly, shedding 13% of their original weight in just two days. Within six days, all mice injected with the virus had died.

In a comparison experiment, similar mice were injected with a contemporary strain of flu, and although the mice lost weight initially, they recovered. Tests revealed that the Spanish flu virus multiplied so rapidly that after four days, mice contained 39,000 times more flu virus than those injected with the more common strain of flu.

The government and military researchers who reconstructed the virus say their work has already provided invaluable insight into its unique genetic make-up and helps explain its lethality. But other researchers warned yesterday the that virus could escape from the laboratory. "This will raise clear questions among some as to whether they have really created a biological weapon," said Professor Ronald Atlas at the centre for deterrence of biowarfare and bioterrorism at the University of Louisville in Kentucky.

Publication of the work and the filing of the virus's genetic make-up to an online database followed an emergency meeting last week by the US National Science Advisory Board for Biosecurity, which concluded that the benefits of publishing the work outweighed the risks. Many scientists remained sceptical. "Once the genetic sequence is publicly available, there's a theoretical risk that any molecular biologist with sufficient knowledge could recreate this virus," said Dr John Wood, a virologist at the National Institute for Biological Standards and Control in Potters Bar.


Oct. 9, 2005
U.S. A Step Behind Bird Flu
Cures Can Be Made, But Time Might Be Against Us
By Sean Alfano

(CBS)   Good news: scientists have not only reconstructed the genetic sequence of the 1918 flu virus, which killed as many as 50 million people, they've learned that it was a bird flu that jumped to humans who then passed it on to each other.

Bad news: there are a lot of similarities between the 1918 virus and the new flu that's killed millions of birds, and at least 60 of the 116 people who've gotten it as it's begun to march across Asia. It's those similarities that have driven this past week's alarming headlines, CBS News correspondent Martha Teichner reports.

"The world is obviously unprepared or inadequately prepared for the potential of a pandemic," says Health and Human Services Secretary Michael Leavitt.

Leavitt was a speaker at an international conference on flu preparedness in Washington attended by 80 nations. Some of whom it seems are way ahead of us in stockpiling the antiviral drug Tamiflu. So if a pandemic is truly on the way, the United States won't have enough.

No doubt, recalling Hurricane Katrina the president was all over the flu issue at his news conference talking about quarantines.

And who best to be able to effect a quarantine: one option is the use of a military that's able to plan and move.

On Friday, President Bush met with drug company officials, urging them to speed up production of flu vaccine.

So why the urgency and why now?

"The lethal capacity of this virus is very, very high, so it's a deadly virus that humans have not been exposed to before. That's a very bad combination," says Dr. Irwin Redlener, director of the National Center for Disaster Preparedness at Columbia University.

"We're only missing one more piece before it becomes a pandemic and that is the ability to be transmitted from person to person as opposed to simply from birds or fowl to humans," Redlener explains.

Which is exactly what happened in the 1918 flu.

Half a million Americans died of it. Maybe 20,000 die in a normal flu season.

In WWI, more soldiers died of the flu than on the battlefield. Living together in close quarters, they were literally attacked in their beds. They got the sniffles one day and were often dead the next.

"People described military camps: they say the bodies were stacked up like cordwood," New York Times science writer Gina Kolata says.

Kolata wrote a book about the 1918 flu. "Never in the recorded history of the world has an infectious disease killed so many people in such a short time," Kolata says.

Most vulnerable were children under 15 and adults between the ages of 20 and 40. For every one person who died, something like 100 got sick.

We told you it was good news that scientists have managed to recreate the 1918 flu. Here's why:

"We can take these genes and sequence them," microbiologist Adolfo Garcia-Sastre says.

Using its genetic signature to clone the virus, Garcia-Sastre and his colleagues at Mt. Sinai school of Medicine in New York are on the verge of determining exactly how a virus mutates and turns deadly, triggering a pandemic.

"We'll be able to predict this type of events," Garcia-Sastre says. Garcia-Sastre added that his team hopes to predict not only when the virus might jump from bird to man and then man to man, but also the lethalness of the flu.

Researchers argue that any risk caused by recreating the virus is offset by what can be learned, but none of this would even be happening if it weren't for an amazing medical detective story.

"This process has been a nine-year effort from that first moment," Dr. Jeffrey Taubenberger says.

Taubenberger, a molecular biologist at the Armed Forces Institute of Pathology in Washington was the lead detective: the man who tracked down the 1918 flu virus and then mapped its genome.

"What we're doing is analyzing a virus right out of the lungs of people who died in the prime of their lives, soldiers who were just in their 20's when they died," Taubenberger explains.

Why soldiers? In a way, thanks to President Lincoln, he became interested in what soldiers were dying of. So, from that day to this, tissue samples have been collected for study. There are now five million little wax blocks and 30 million slides.

When we first met Dr. Taubenberger in 1999, he explained that he had thought, maybe, somewhere in this amazing archive, he could find a sample that contained the 1918 flu virus.

He found not one, but two.

Enter Dr. Johann Hultin, a retired pathologist from San Francisco. In 1951, he had tried and failed to extract the virus from flu victims frozen into the ground in Alaska. The technology simply wasn't sophisticated enough then, but when Hultin read about Taubenberger's discovery, he tried again.

This time he found the bodies decomposed. All except one.

"That was a great moment. Like that," Hultin snaps his finger, "I knew it."

The virus in the lung tissue matched the two soldiers', proving it was the 1918 flu.

"The long-term goal would be to apply this information in a way that ultimately might be able to prevent a pandemic from ever happening again," Taubenberger says.

But what if it does? A copy of a Bush administration plan for dealing with a flu pandemic was just leaked to the New York Times. It outlines a worst case scenario: 1.9 million Americans dead and 8.5 million hospitalized.

It talks about a domestic vaccine production capacity of 600 million doses within 6 months, more than 10 times the present capacity.

"There is an h5n1, an avian flu, bird flu vaccine. They first made a two million dose batch and now they're doing a 20 million dose batch," says Doris Bucher.

A far cry from 600 million. Bucher heads a lab at the New York Medical College that creates flu vaccines.

"The thing about flu is that it's so mutable," Bucher says.

Which is why making a vaccine requires tailoring it precisely to whatever form the flu virus finally takes and that requires time, months we may or may not have.

"We started from zero five weeks ago to all this hot, hot spotlight on pandemic flu, but we're not going to be ready," Dr. Irwin Redlener says.

If we're lucky, it won't happen. At least, not this year, and we buy ourselves time to be ready. We can only hope.
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-vaccine+chemtrail Bioweapon
: Anti_Illuminati December 05, 2009, 04:04:57 PM

Natural Products and Lifestyle - Their Potential Role in a Bird Flu Pandemic

by Dr Robert Verkerk (more info)
listed in medical conditions, originally published in issue 132 - February 2007

Where Are We in the Winter of 2006?

Many of us have heard about the risk of a flu pandemic, initiated from the H5N1 virus in birds, over a year ago. Reports in the media made headline news for a few months following October 2005. The reports then went quiet through much of the summer, but with the advent of the northern winter, news reports are again hotting up.

There is now increasing evidence that the H5N1 possesses remarkably dynamic powers of evolution, and is continuing to evolve new genetic clades (groups) and sub-clades, meaning that much of the vaccine development research undertaken since 2004 is next to worthless.[1] The recent changes in the genetics of the virus have caused the World Health Organization (WHO) to change its candidate virus strains in August 2006 for the first time since 2004.[2] Adding insult to injury, significant parts of the existing vaccine stockpiles that have been accumulated since 2005 are beginning to lose their potency.[3]

Even the United States, which tends to be a little ahead of the curve in terms of developing plans to protect its population, the vaccine and anti-viral drug stockpile is looking somewhat inadequate. A report just released by the US Department of Health and Human Services indicates that only five million doses of vaccine will be available by the end of 2006 – this equates to just a single dose for 1.7% of the US population. In the same timeframe, there will only be enough anti-viral drugs (Tamiflu and Relenza) for 25% of its population.[3]

Adding insult to injury, the Royal Society, represented by the likes of Sir John Skehel, one of the most eminent virologists in the world, said last November that the UK is simply not ready for a pandemic, and much more is needed by way of preparedness.[4-5] The UK, rather typically, is even further behind the US. In a recent collaborative study by John Hopkins Bloomberg School of Public Health and Ben Gurion University Israel, involving analysis of pandemic plans from 19 developed and 26 developing countries which contain around two-thirds of the world’s population, researchers found that 62% of the plans prioritized flu vaccination, while almost half favoured anti-viral medications, such as Tamiflu.[6]

It is becoming increasingly evident that reliance on pharmaceuticals as the central plank of preparedness plans is going to lead to catastrophe. Anti-viral drugs have unknown efficacy in a pandemic; resistance is likely the potential for neuropsychiatric effects associated with Tamiflu use which has already been reported.[7] In relation to vaccines, they will always be delayed in their arrival, they may need to be developed for multiple strains, they will always be scarce given manufacturing limitations, and they also may be ineffective.

With all this focus on potentially worthless pre-pandemic vaccines and anti-viral drugs of unknown efficacy, and potentially serious side-effects, the pharmaceutical industry may be the clear winner, even before a pandemic has occurred. Tamiflu is made by Roche, and Relenza by GlaxoSmithKline. A small cluster of companies make the vaccines.

How Much of a Threat is H5N1 to Humans?

Given the relatively trivial number of confirmed human cases and deaths (258 cases confirmed by WHO, resulting in 153 deaths [59% fatality rate]),[8] many have chosen to think of avian flu as hype perpetuated by over zealous media and greedy pharmaceutical companies, keen to peddle vaccines and anti-viral drugs.

It is easy to lay the blame for all this money-making on nature – and wild birds in particular. However, one of the world’s leading virologists, Dr Robert Webster from St Jude’s Children’s Research Hospital in Memphis, Tennessee, US, who has been focusing his recent research on H5N1, points his finger in more than one direction, saying, “The global poultry industry is the main spreader of H5N1, but migratory birds have certainly played a role”.[9]

Prof Neil Ferguson, a leading epidemiologist from Imperial College London, has modelled the epidemiology of avian influenza that could arise from a single infected human. The model (Figure 1)[10] shows that in the first 30 days of the pandemic, virtually no cases of infection would be evident, despite extremely high transmission rates, yet peak infection and cases would occur around 60 days after the initial single infection. This emphasizes just how brutal a pandemic could be; of course, as we have seen already, it is more or less impossible to predict the actual pathogenicity of the final pandemic strain(s).

The significance of each human case is widely misunderstood by those sceptical of the pandemic risk, who have generally made judgements based on the comparative rarity of human cases. As pointed out by the WHO Secretariat at last year’s World Health Assembly in Geneva, “Each human case gives the virus an opportunity to develop into a form that spreads efficiently and sustainably among humans, at which point a pandemic is expected to start”.[11]

As we enter another winter in northern Europe, the risks increase rather than decrease. This is due to such factors as the continuing evolution of the virus, migratory patterns of asymptomatic wild birds, and the wide scale, and often illegal use of vaccines in poultry populations, as well as the movement of the virus into non-avian hosts. Vaccines used not only kill the virus, they may also contribute to untoward genetic changes and increase the number of poultry that are asymptomatic, so increasing the risk of undiagnosed transmissions.

International experts are keeping a particularly close watch on China, Indonesia and Thailand as the countries where a flu pandemic seems most likely to be initiated.

Apart from the health consequences, the economic consequences of a pandemic could be disastrous. Professor Warwick McKibbin and Dr Alexandra Sidorenko, from the Lowy Institute and Australian National University in Australia, have estimated that the pandemic might kill 142 million people and wipe about US$4.4 trillion from economic output, according to a worst-case scenario. Even the mild scenario projected loss of 1.4 million lives and close to 0.8% of GDP (approximately US$330 billion) in lost economic output.[12]

Why is the H5N1 Virus Potentially so Lethal?

In short, people who are infected with the H5N1 virus undergo an extraordinarily severe immune response, which appears, at the present time, to have a more than 50% chance of leading to death within a matter of days. This immune response is initiated by pro-inflammatory cytokines from the cell-mediated (adaptive) side of the immune system. This hyper-induction of cytokines causes massive respiratory distress, and death is primarily the result of severe viral pneumonia. However, the recent isolation of the virus in extra-pulmonary sites, as well as a wide diversity of symptoms evident in lethal cases,[13] suggests other mechanisms may also be active.

Of critical importance, however, is the fact that lethal H5N1 influenza viruses, unlike other human, avian and swine influenza viruses, are resistant to the anti-viral effects of interferons and tumour necrosis factor (TNF)-alpha (Th-1 pro-inflammatory cytokines).[15]

It appears that those with the healthiest immune systems, notably the young, are most likely to die as a result of this immune system over-response. Let us not forget that during the 1918 H1N1 pandemic, most of the 50 million or so deaths around the world were among 18 to 40 year-old men, generally viewed as the fittest and strongest members of any population.[10]

Could Natural Products Save the Day?

Regulators and the orthodox medical community around the world have generally scorned the use of natural health products for prevention or treatment of serious diseases, this being regarded widely as the sole preserve of licensed medicines. This view is epitomized by two recent scathing attacks on complementary medicine by Professor Michael Baum (May 2006)[16] and Professor Jonathan Waxman (November 2006)[17] in which both oncologists claim, in profound error I should add, that there is no scientific evidence of any benefits for complementary medicine or food supplement products.

In contrast, it should be recognized, as stressed in a 2005 report by the House of Common Health Committee, The Influence of the Pharmaceutical Industry,[18] that the drugs companies have for decades ‘cosied-up’ with regulators, creating, in the process, licensing regimes that allow ring-fencing of drug interests to the exclusion of others. The British Medical Journal’s own website Clinical Evidence reports that, of the 2,404 orthodox medicine treatments they have surveyed, only 15% are rated as beneficial, while 47% are of unknown effectiveness![19] In my view, human ingenuity is such that in the case of an emergency, real needs come to the fore, and it is much more likely that Big Pharma’s treasured rule book might get pushed to one side. The US government has already taken a very keen interest in one UK-developed and patented zinc product, for which it is funding further research, and it seems likely that use of such natural products will be advocated by more enlightened governments during times of emergency.

Conspicuously absent from present strategies being considered by health authorities around the world, is the potential use of prophylactic, natural product-based approaches designed to modulate immune system function in the event of infection. This is, in part, because there is relatively very little data available on the efficacy of natural products specifically on H5N1, and none, as far as I am aware, on H5N1 infected humans. That which is available, such as on the patented zinc product indicated above, is bound by confidentiality agreements and as yet unpublished. The work has been conducted both in-vitro and in-vivo, in a mouse model, using the very same US National Institutes of Health laboratory in which the anti-viral drug Tamiflu was tested. There has also been some other work, which I believe has been mainly carried out within in-vitro systems, using a black elderberry formulation.

Aside from this, any other assertions made about natural products, and their potential role in the mitigation of H5N1 is speculative, and made on the basis of knowledge of the mechanism of infection by H5N1 and the progression of the resulting disease in humans, as well as the biochemical, immunological and pharmacological nature of particular natural products. Justification for the potential use of a diverse range of vitamins, minerals, herbal and fungal products have been collated within the report: The Pivotal Role for Natural Products in Countering an Avian Influenza Pandemic, released last April by the Alliance for Natural Health (ANH) Avian Influenza Expert Committee, of which I am a member. The report is available free of charge online.20 The report was precipitated by a direct request by the WHO last February to provide an opinion from the British Society of Ecological Medicine and the ANH, on those natural products and dosages that may be candidates for immune system modulation in the event of a high pathogenicity H5N1 pandemic.

In my view, should a pandemic be sparked in the near future, it is going to be down to practitioners, consumers and other advocates of natural health approaches, to publicize what individuals can do to increase their chances of defending themselves and their families in the event of a pandemic. If one government, such as the United States, takes a lead on the basis of their own research and knowledge of a given product, this will be very helpful and may trigger some other governments to follow suit.

Summary of the Potential Role of Natural Products

The following information is derived from some of the recommendations given in the thoroughly referenced ANH report, The Pivotal Role for Natural Products in Countering an Avian Influenza Pandemic.[20] The report proposes protocols for three types of situations:
1.    Prophylaxis;
2.    Self-treatment;
3.    Medical treatment (including intravenous use of nutrients) which have been developed in collaboration with the British Society of Ecological Medicine.

This information is not presented as medical advice, but rather as a representation of the current state of scientific knowledge on the potential role of natural products in the event of highly pathogenic H5N1 pandemic.

•    Zinc deficiency is a very well-established cause of immune system imbalance, and the vast majority of people in the world are zinc deficient. The amount of zinc from the diet, or from multivitamin and mineral tablets alone, tends not to provide the body with sufficient zinc, owing to the way in which zinc complexes with other compounds, especially phytates in cereals. Liquid (ionic) zinc supplements taken between meals appear to be a better option. One such supplement, shortly to be commercially available in the US, has undergone extensive testing, including in mouse models with the H5N1 virus, and may be one of the best options available at present;

•    The short half-life of vitamin C means that vitamin C should be taken at around three-hourly intervals throughout the day. This presents problems at night time, so it can be useful to take a high strength (e.g. 1500 mg) slow release formulation before going to bed, which can be taken again during the course of the night if a person wakes. Dosage should be increased to bowel tolerance, and then should be backed off slightly. The bowel tolerance level is likely to alter considerably between prophylaxis and treatment situations, owing to the considerably greater demand by the body during infection;

•    High doses of vitamin A, or better still, pro-vitamin A mixed carotenoids (containing 60mg beta-carotene for prophylaxis or double this dosage for self-treatment) will help to modulate the immune system;

•    Extremely high doses of vitamin B12 (20-100mg), delivered intravenously by medical doctors, may be able to play an important role in medical treatment of those infected by H5N1. Such dosages have been used for treatment of haemorrhagic shock and cyanide poisoning and, based on scientific understanding of B12’s action, are likely to be able to quell cytokine storms in infected individuals;

•    Certain botanical and fungal products may be very helpful in the modulation of the immune system, while others may hyper-induce pro-inflammatory cytokines, particularly if excessive dosages are consumed. This includes products such as black elderberry and Echinacea. Nutrients such as resveratrol (from grapes) and beta-glucans (from maitake mushrooms, oats, etc.) are of particular interest. Responsible manufacturers will likely make very clear statements over recommended dosages in the event of a pandemic to help consumers to avoid over-dosing;

•    All interventions should be undertaken in conjunction with dietary and lifestyle approaches designed to optimize immune system function. They include proper hydration, consumption of a varied, high fruit and vegetable content, high protein and complex carbohydrate, low saturated fat diet, as well as the inclusion of moderate (but not excessive) exercise. These sorts of recommendations, although well-understood by complementary medicine practitioners, are still not practised by the majority, and of course will be even more challenging during a pandemic. Ideally they should be initiated at least two months prior to being exposed to the virus.

In Conclusion

The dosages of micronutrients likely to be required either in prophylaxis, but especially for treatment, generally far exceed the relevant Recommended Daily Allowance (RDA), and are, in the main part, orders of magnitude greater than those contemplated by the European Commission and various international bodies working to set EU-wide maximum permitted levels for food supplements (under Article 5 of the EU Food Supplements Directive). This will come as no surprise to many, as the levels being considered by the authorities are not designed to either prevent or treat disease. The regulators appear to be doing everything in their capacity to make therapeutic dosages the exclusive domain of licensed medicines.

Why the need for such apparently high doses? Firstly, the science being used to establish so-called safe upper levels and maximum permitted levels is deeply flawed and suggests dosages that are unnecessarily low for many nutrients.[21] Secondly, the levels required to help the body once under attack by infectious agents, tend to be much greater than those required for normal physiological maintenance. This might prompt you to ask: why are concentrated forms of food products that happen to be delivered in capsules, tablets or powders, as food supplements, treated so differently from healthy foods which are well-acknowledged to reduce the risk of a wide range of important diseases, including cancer and cardiovascular disease?

It is possible that the imminent threat of a human form of bird flu may just help to sharpen the minds of orthodox doctors, governments and regulators. Failing this, consumers will do what they need to do, to protect themselves and their families. As with so many paradigm shifts, this one is most likely to be driven by need and consumer demand.

The first line of defense should always be trying to avoid infection in the first place. Approaches such as social isolation, school and workplace closures and travel restrictions have accordingly already been proposed.[22-23] Prophylactic approaches accessible to all should be the second most important consideration – and natural products, freely available to consumers as food/dietary supplements or as homoeopathic remedies, are in our reckoning the best options we have.

Once a pandemic is triggered, it seems that the anti-natural product lobby might have to learn to accept that it is not so easy to separate humans from their natural heritage. As a species, we have always had a tendency to look to nature for solutions. Even the pharmaceutical industry has built most of its immense profits by tweaking molecules originally sourced from nature. Millions of people will inevitably seek out natural approaches to give themselves the best opportunity of protecting both themselves and their loved ones. Practitioners owe it to their clients and patients to keep themselves as well-informed as they can.

1.    WHO working group. Influenza research at the human and animal interface. Report from 21-22 September workshop. World Health Organization. Geneva. 2006.
influenza/WHO_CDS_EPR_GIP_2006_3C.pdf [last accessed 25 November 2006].
2.    WHO advisory notice of H5N1 candidate viruses. 18 August 2006.
avian_influenza/guidelines/h5n1virus2006_08_18/en/index.html [last accessed 25 November 2006].
3.    Department of Health and Human Services. Pandemic Planning Update III. Report from Secretary Michael O Leavitt. DHHS. Washington. 13 November 2006. [last accessed 25 November 2006].
4.    BBC News. Report: Experts call for better flu plans. 20 November 2006. health/6158310.stm [last accessed 21 November 2006].
5.    The Royal Society/The Academy of Medical Sciences. Pandemic Influenza: science to policy. Policy document 36/06. The Royal Society. London. ISBN-13: 978 0 85403 635 6.
6.    Uscher-Pines L, Omer SB, Barnett DJ, Burke TA and Balicer RD. Priority setting for pandemic influenza: An analysis of national preparedness plans. PLoS Med 3 (10): e436. 2006.
7.    US Food and Drug Administration. Drug Alerts 2006; Tamiflu. htm#tamiflu [last accessed 25 November 2006].
8.    World Health Organization. Cumulative Number of Confirmed Human Cases of Avian Influenza A/(H5N1) Reported to WHO. 13 November 2006. ( influenza/country/cases_table_2006_08_14/en/index.html) [last accessed 21 November 2006].
9.    BBC News. Report: Wild Bird Role in Flu ‘Unclear’. 31 May 2006. 5032904.stm [last accessed 21 November 2006].
10.    House of Lords. Science and Technology Committee. Pandemic Influenza. Fourth Report of Session. 2005-2006. The Stationary Office Ltd. London. 2006.
11.    WHO Secretariat. Strengthening pandemic-influenza preparedness and response. 1 December 2005. B117_5-en.pdf [last accessed 25 November 2006].
12.    McKibbin WJ and Sidorenko AA. Global Macroeconomic Consequences of Pandemic Influenza. Lowy Institute for International Policy Report. Lowy Institute. Sydney. 79pp. ( [last accessed 20 March 2006].
13.    Chotpitayasunondh T, Ungchusak K, Hanshaoworakul W, Chunsuthiwat S, Sawanpanyalert P, Kijphati R, Lochindarat S, Srisan P, Suwan P, Osotthanakorn Y, Anantasetagoon T, Kanjanawasri S, Tanupattarachai S, Weerakul J, Chaiwirattana R, Maneerattanaporn M, Poolsavathitikool R, Chokephaibulkit K, Apisarnthanarak A and Dowell SF. Human Disease from Influenza A (H5N1). Thailand. 2004. Emerging Infectious Diseases 11: 201-9. 2005.
14.    Wong SSY and Yuen K. Avian influenza virus infections in humans. Chest. 129: 156-168. 2006.
15.    Seo SH, Hoffmann E and Webster RG. Lethal H5N1 influenza viruses escape host anti-viral cytokine responses. Nature Medicine. 8: 950-4. Epub. 26 Aug 2002.
16.    Times Online. Full letter: doctor’s campaign against alternative therapies (by Michael Baum and others). 0,,8122-2191985,00.html [last accessed 25 November 2006].
17.    Waxman J. Shark cartilage in the water (BMJ/Personal Views). BMJ 333: 1129. 2006.
18.    House of Commons Health Committee. The Influence of the Pharmaceutical Industry. The Stationary Office. London. cmselect/cmhealth/42/42.pdf [last accessed 24 November 2006].
19.    BMJ Clinical Evidence website: How much do we know. knowledge.jsp [last accessed 25 November 2006].
20.    Alliance for Natural Health Avian Influenza Expert Committee. The Pivotal Role for Natural Products in Countering an Avian Influenza Pandemic. April 2006. Alliance for Natural Health. Dorking. UK. ANHwebsiteDoc_232.pdf [last accessed 25 November 2006].
21.    Alliance for Natural Health (ANH) submission to FAO/WHO Nutrient Risk Assessment Project. December 2003. and ANH Submission to the European Commission’s Consultation on the Setting of Maximum Permitted Levels. September 2006. .pdf [last accessed 25 November 2006].
22.    Ferguson NM and Cummings DA. Strategies for Mitigating an Influenza Pandemic. Nature. 442: 448-52. Epub. 2006.
23.    Wu JT, Riley S, Fraser C and Leung GM. Reducing the Impact of the Next Influenza Pandemic using Household-based Public Health Interventions. PLoS Med. 3: e361. 2006.
: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-vaccine+chemtrail Bioweapon
: Satyagraha December 05, 2009, 04:55:02 PM
Although written for the Bird Flu false flag, this article has good info very relevant to the current H1N1 Hybrid Phase2 Bioweapon that the NWO has unleased on us all... the similarities to the H5N1 symptoms are striking, and the natural anti-virals and remedies are extremely important for all of us to include in our daily nutritional intake...

Summary of the Potential Role of Natural Products

The following information is derived from some of the recommendations given in the thoroughly referenced ANH report, The Pivotal Role for Natural Products in Countering an Avian Influenza Pandemic.[20] The report proposes protocols for three types of situations:
1.    Prophylaxis;
2.    Self-treatment;
3.    Medical treatment (including intravenous use of nutrients) which have been developed in collaboration with the British Society of Ecological Medicine.

This information is not presented as medical advice, but rather as a representation of the current state of scientific knowledge on the potential role of natural products in the event of highly pathogenic H5N1 pandemic.

•    Zinc deficiency is a very well-established cause of immune system imbalance, and the vast majority of people in the world are zinc deficient. The amount of zinc from the diet, or from multivitamin and mineral tablets alone, tends not to provide the body with sufficient zinc, owing to the way in which zinc complexes with other compounds, especially phytates in cereals. Liquid (ionic) zinc supplements taken between meals appear to be a better option. One such supplement, shortly to be commercially available in the US, has undergone extensive testing, including in mouse models with the H5N1 virus, and may be one of the best options available at present;

•    The short half-life of vitamin C means that vitamin C should be taken at around three-hourly intervals throughout the day. This presents problems at night time, so it can be useful to take a high strength (e.g. 1500 mg) slow release formulation before going to bed, which can be taken again during the course of the night if a person wakes. Dosage should be increased to bowel tolerance, and then should be backed off slightly. The bowel tolerance level is likely to alter considerably between prophylaxis and treatment situations, owing to the considerably greater demand by the body during infection;

•    High doses of vitamin A, or better still, pro-vitamin A mixed carotenoids (containing 60mg beta-carotene for prophylaxis or double this dosage for self-treatment) will help to modulate the immune system;

•    Extremely high doses of vitamin B12 (20-100mg), delivered intravenously by medical doctors, may be able to play an important role in medical treatment of those infected by H5N1. Such dosages have been used for treatment of haemorrhagic shock and cyanide poisoning and, based on scientific understanding of B12’s action, are likely to be able to quell cytokine storms in infected individuals;

•    Certain botanical and fungal products may be very helpful in the modulation of the immune system, while others may hyper-induce pro-inflammatory cytokines, particularly if excessive dosages are consumed. This includes products such as black elderberry and Echinacea. Nutrients such as resveratrol (from grapes) and beta-glucans (from maitake mushrooms, oats, etc.) are of particular interest. Responsible manufacturers will likely make very clear statements over recommended dosages in the event of a pandemic to help consumers to avoid over-dosing;

•    All interventions should be undertaken in conjunction with dietary and lifestyle approaches designed to optimize immune system function. They include proper hydration, consumption of a varied, high fruit and vegetable content, high protein and complex carbohydrate, low saturated fat diet, as well as the inclusion of moderate (but not excessive) exercise. These sorts of recommendations, although well-understood by complementary medicine practitioners, are still not practised by the majority, and of course will be even more challenging during a pandemic. Ideally they should be initiated at least two months prior to being exposed to the virus.

: Re: J. Taubenberger & T. Tumpey=BIOTERRORISTS-vaccine+chemtrail Bioweapon
: TahoeBlue January 07, 2013, 03:47:35 PM
sociostudent  - Taubenberger: More of a psychopathic evil scientist than Pianka  (