CDC Admits 30 Million Possibly at Risk For Cancer Due To Polio Vaccine SV40

[larsonstdoc]

http://www.thelibertybeacon.com/2013/07/12/cdc-admits-as-many-as-30-million-americans-could-be-at-risk-for-cancer-due-to-polio-vaccine/

Do vaccines cause cancer? Well Straight from the horses mouth, The CDC says it just may be so … but after 50 years they state more studies are needed (REALLY?).

The Centers for Disease Control and Prevention (CDC) posts on its own website the concern that as many as 30 million Americans could be at risk for cancer after receiving a Polio vaccination during the 1955 – 1963 time frame. This possibility exists because the vaccine in question was found to be contaminated with the SV40 virus. Most Americans received multiple doses of this vaccine that was administered to almost 100 million people.

It is stated that after the discovery (in 1960), any newly manufactured Polio vaccine was free of this virus (it took 3 years). No information is available as to exactly how much of the vaccine was tainted at the time, nor is there any information as to the controls put in place to insure all the tainted vaccine was effectively recalled.

[TahoeBlue]

A designed expiration date...
http://www.youtube.com/watch?v=O5MDGMvrSJc
Blade Runner - I want more life

http://www.cdc.gov/vaccinesafety/updates/archive/polio_and_cancer_factsheet.htm
Cancer, Simian Virus 40 (SV40), and Polio Vaccine Fact Sheet

•SV40 is a virus found in some species of monkey.

•SV40 was discovered in 1960. Soon afterward, the virus was found in polio vaccine.

•More than 98 million Americans received one or more doses of polio vaccine from 1955 to 1963 when a proportion of vaccine was contaminated with SV40; it has been estimated that 10–30 million Americans could have received an SV40 contaminated dose of vaccine.

•SV40 virus has been found in certain types of cancer in humans, but it has not been determined that SV40 causes these cancers.

•The majority of scientific evidence suggests that SV40-contaminated vaccine did not cause cancer; however, some research results are conflicting and more studies are needed.

•Polio vaccines being used today do not contain SV40. All of the current evidence indicates that polio vaccines have been free of SV40 since 1963.

Additional Facts

•In the 1950s, rhesus monkey kidney cells, which contain SV40 if the animal is infected, were used in preparing polio vaccines. Because SV40 was not discovered until 1960, no one was aware in the 1950s that polio vaccine could be contaminated.

•SV40 was found in the injected form of the polio vaccine (IPV), not the kind given by mouth (OPV).

•Not all doses of IPV were contaminated. It has been estimated that 10–30 million people actually received a vaccine that contained SV40.

•Some evidence suggests that receipt of SV40-contaminated polio vaccine may increase risk of cancer. However, the majority of studies done in the U.S. and Europe which compare persons who received SV40-contaminated polio vaccine with those who did not have shown no causal relationship between receipt of SV40-contaminated polio vaccine and cancer.

More Information
•For in-depth information about SV40, polio vaccine, and cancer, see our frequently asked questions.
•National Immunization Hotline:
 English 1 (800) 232-2522
 Spanish 1 (800) 232-0233

Page last modified: October 22, 2007
 Content source: Immunization Safety Office

http://curezone.com/forums/fm.asp?i=1015019
... And the rest not mentioned by CDC ... SV40

http://www.sfgate.com/health/article/New-documents-show-the-monkey-virus-is-present-in-2897194.php
New documents show the monkey virus is present in more recent polio vaccine
William Carlsen, Chronicle Staff Writer
Published 4:00 am, Sunday, July 22, 2001
...

Scientists discovered SV40 in the Salk polio vaccine in 1960. By then as many as 30 million Americans had been given injections of the SV40-tainted polio vaccine, which was first licensed in 1955.

In recent years more than 60 scientific studies have found SV40 in rare human brain, bone and lung-related cancers, the same kinds of tumors the virus caused in laboratory animals. Some scientists believe SV40 may play a role in causing those cancers.

One of the biggest mysteries, however, is why SV40 has been found in tumors removed from people who never received the contaminated Salk vaccine.

Researchers have several theories for how the virus could have spread from those infected through the Salk vaccine: in transmission from mother to fetus or through breast milk; through sexual activity or a flu-like virus.

But the Lederle documents, which were obtained by Philadelphia attorney Stanley Kops in litigation not related to SV40, raise the possibility the virus might have been transmitted by contaminated oral vaccine, licensed for production in 1962.
...

The documents include:

-- A November 1961 memo saying the virus was found in three of 15 lots of vaccine. According to the memo, Dr. Roderick Murray, head of the government's program to ensure vaccine purity, allowed the lots to be released.

To comply with the removal order, Lederle had switched from rhesus monkeys, which are natural hosts for SV40, to African green monkeys, supposedly free from SV40. However, the memo notes that SV40 was found in 10 percent of the green monkeys.
...
"The vaccine manufacturers and the government need to disclose what really happened," said Kops. "Without the facts, (scientists) will continue to look in the wrong places to explain how people were infected with SV40 after 1961."
...
At a 1997 conference, however, a company representative outlined the series of tests the company uses to detect SV40 contamination. The company also says that it uses antiserum to neutralize any SV40 in the "master seeds."

But it is not clear whether these procedures were in place in the years after the U.S. government issued its directive.
...
Last year, a lawsuit was filed in Los Angeles against Lederle by the parents of 2 1/2-year-old Alexander Horwin who died of a brain tumor that later tested positive for SV40. The suit claims that the tumor was caused by SV40 and that he became infected through a 1997 oral polio vaccine.
...

In 1970, surgeons removed a large brain tumor from 2-year-old Mark Moreno. He since has undergone five more surgeries and now wears a protective helmet over the large opening in his cranium where bone grafts never took. Moreno, now 33, lives with his mother and requires daily assistance.

Recent tests show Moreno's tumor was riddled with SV40, according to the lawyers.

Eileen Moreno, Mark's mother, believes her son's brain tumor was caused by SV40 and that he was infected through the oral polio vaccine in 1968.

...

MacLachlan said he finds it "incredible" that the government hasn't comprehensively investigated the possibility of SV40 contamination of the oral vaccine.
...
Simian virus Q&A Q: How widespread is the SV40 infection?

A: Scientists and government health officials don't know, because no comprehensive studies have addressed the question. What is known is that during the 1950s and '60s, at least 10 million to 30 million Americans -- and more than 100 million people worldwide -- were given SV40-contaminated polio vaccine. The virus also has been found in people who did not receive contaminated vaccine.

Q: Can I be tested for SV40?

A: An accurate blood test does not exist. Current antibody blood tests can be inaccurate, scientists say, because they also may detect the presence of closely related viruses, and SV40 may be present at such a low level that no antibodies are produced. Researchers are working to create an effective test.

[TahoeBlue]

Research still ongoing!: 
SV40 appears to be contagious like HIV plus fecal-oral transmission route

"the haematic [blood], sexual and orofecal routes of transmission are likely to be responsible for SV40 horizontal infection in humans"

http://www.bcm.edu/imbs/?PMID=2046
Janet S. Butel, Ph.D

Distinguished Service Professor and Chair, Department of Molecular Virology & Microbiology
 Ph.D., Baylor University College of Medicine
 Postdoctoral, Baylor College of Medicine

Research Interests:

The Butel laboratory is interested in polyomavirus pathogenesis of infections and disease, with a primary focus on polyomavirus SV40. Originally isolated from monkeys, SV40 is a small DNA virus that is able to transform cells in culture and induce tumors in rodents. As a model tumor virus, SV40 has provided many fundamental insights into the molecular basis of carcinogenesis.

The large tumor antigen (T-ag) of SV40 is the major transforming protein of the virus, responsible for tumor causation in rodents and transformation of many cell types in culture. It is a complex protein that possesses multiple functions important for replicating the viral DNA and for dysregulating cell cycle control. Sequence analysis of viral isolates has revealed differences in the structure of the noncoding viral regulatory region as well as the existence of a variable region at the C-terminus of T-ag that can classify SV40 strains into genogroups.

We have developed the Syrian golden hamster small animal model to study SV40 pathogenesis of infection and disease. Recent findings include the significant effect of the structure of the viral regulatory region on both oncogenic potential and vertical transmission in vivo. There was no effect on transforming activity in vitro, indicating that strain-specific factors affect virus–host interactions that are not detectable using cultured cells. The hamster model is being used to address the effect of SV40 genetic variations on patterns of viral infection that predispose to disease development.

Research in the last several years has established that authentic SV40 can cause human infections and is associated with certain types of human tumors, including brain tumors and lymphomas.

New findings related to human infections include the fecal excretion of polyomaviruses by humans, indicating a probable fecal–oral route of transmission;

the detection of SV40 in normal and malignant lymphoid-rich tissues, suggesting that lymphoid cells are important in the pathogenesis of SV40 infections;

and the variable frequency of SV40-positive lymphomas in two urban populations with different demographics, emphasizing that SV40 infection and disease likely reflect population differences.

Current research includes an analysis of SV40 effects on human lymphocytes and the role of SV40 microRNA in pathogenesis of infections.

Studies of the newly discovered human cancer virus, Merkel cell polyomavirus, are also in progress.

http://www.ncbi.nlm.nih.gov/pubmed/16626024
Polyomaviruses and human diseases.

Abstract

Polyomaviruses are small, nonenveloped DNA viruses, which are widespread in nature.

In immunocompetent hosts, the viruses remain latent after primary infection. With few exceptions, illnesses associated with these viruses occur in times of immune compromise, especially in conditions that bring about T cell deficiency. The human polyomaviruses BKV and JCV are known to cause, respectively, hemorrhagic cystitis in recipients of bone marrow transplantation and progressive multifocal leukoencephalopathy in immunocompromised patients, for example, by HIV infection
...

http://www.vacfacts.info/scientific-proof-that-the-known-cancer-causing-sv40-virus-a-previous-contaminant-in-the-polio-vaccine-is-obviously-either-contagious-or-the-virus-is-still-in-the-vaccines.html

Scientific proof that the known cancer causing SV40 virus, a previous contaminant in the polio vaccine, is obviously either contagious; or the virus is still in the vaccine/s.

...

http://www.biomedcentral.com/content/pdf/1750-9378-2-13.pdf
Simian virus 40 in humans
...
 To date, the prevalence of SV40 infections in humans is not known. Recent studies, based on PCR and serological techniques, indicate that SV40 infection occurs both in children and adults. (i) SV40 DNA sequences have been detected in normal and neoplastic tissues of people either too young (1 to 30 years) or too old (60 to 85 years) to have been vaccinated with SV40-contaminated anti-polio vaccines [19,33,76-81].

This finding may also explain the lack of difference in cancer incidence between individuals vaccinated with SV40-contaminated and SV40-free anti-polio vaccines [82]. (ii) SV40 sequences and Tag were detected in blood and sperm specimens from normal individuals and oncologic patients [80,81,83-88] and in lymphoblastoid cells [32]. These results suggest that PBMCs could be a reservoir and vehicle of SV40 spreading in the tissues of the host and among the individuals. (iii) SV40 sequences were found in urine and stoole samples, from children and adults [84,89,90], indicating that the haematic, sexual and orofecal routes of transmission are likely to be responsible for SV40 horizontal infection in humans.

http://www.ncbi.nlm.nih.gov/pubmed/23621738
Mikrobiyol Bul. 2013 Apr ;47(2):362-81.

[New, newer, newest human polyomaviruses: how far?].
...
Due to the known transforming capacity of SV40, it was initially thought that the incidence of cancer could increase following the administration of SV40-contaminated polio vaccines, however advanced studies yielded inconsistent results, without any evidence to conclude whether or not the contaminated polio vaccine caused cancer.

Several studies have reported the detection of SV40 genome in some of the human tumors, as well as in the clinical samples of healthy subjects.

In addition SV40 seropositivity was reported in human populations although in low rates (2-10%).

These data have raised the possibility that SV40 infects humans and circulates in human populations unrelated to being exposed to the vaccine.

The discovery of the first human polyomaviruses was in 1971 independently from each other, one was BK virus (BKPyV) isolated from the urine sample of a renal transplant patient, and the other was JC virus (JCPyV) isolated from the brain tissue of a patient with progressive multifocal leukoencephalopathy, and both were named after the patients' initials.

BK and JC viruses were the only well-known human polyomaviruses throughout 36 years, however dramatical increase in number of newly identified human polyomaviruses was recorded in the last six years due to the use of sophisticated molecular methods and new-generation sequencing technologies.

In 2007, two new HPyVs were identified independently from nasopharyngeal aspirates of children with acute respiratory tract infections; one was KI (Karolinska Institute) and the other was WU (Washington University) polyomaviruses, named after the initials of institutes which they were first described.

In 2008, the fifth HPyV namely Merkel cell polyomavirus (MCPyV) was isolated from the skin tumor sample of a patient with Merkel cell carcinoma.

In 2010, three other novel human polyomaviruses were discovered, two were from skin samples of healthy subjects (HPyV-6 and HPyV-7), and one (Trichodysplasia Spinulosa-associated virus; TSPyV) from keratotic spicule sample of a heart-transplanted patient.

Another new HPyV was identified in 2011 named HPyV-9, from the blood and urine samples of an asymptomatic patient with kidney transplant.

Most recently, three new HPyVs have been sequentially discovered during the last quarter of 2012. The 10th HPyV (HPyV10) was identified in condyloma samples of an immunocompromised patient with WHIM syndrome (Wart, Hypogammaglobulinemia, Infections, Myelokathexis), 11th virus was isolated from stool sample of a healthy child from Malawi (Malawi polyomavirus; MWPyV), and 12th was described from fecal sample of a diarrheal child from Mexico (Mexico polyomavirus; MXPyV). The whole genome sequence analysis of HPyV10, MWPyV and MXPyV pointed out that they are closely related viruses.

The last novel polyomavirus, namely Saint Louis polyomavirus (STLPyV) has been reported in a study published on February 2013, identified from the stool sample of a healthy child.

Seroepidemiological studies indicated that most of the novel HPyVs are highly prevalent (average rate: 40-80%) worldwide and likely acquired asymptomatically during childhood, similar to the old ones, BKPyV and JCPyV. However data about HPyV10, MWPyV, MXPyV and STLPyV are not enough as they have been discovered most recently. Similarly, little is known about the pathogenesis, route of infection and the relationship with clinical diseases of novel HPyVs except MCPyV and TSPyV which are known to be responsible for Merkel cell carcinoma and trichodysplasia spinulosa, respectively. The expanding repertoire of human polyomaviruses made us think that many others will be uncovered in the future thanking to the advances in molecular methods. In this review, recent developments subjecting new human polyomaviruses have been summarized.

[TahoeBlue]

http://www.sv40foundation.org/Types.html

Types of SV40 Associated Cancers

Below are types of human cancers in which SV40 has been found. By clicking on the name, you will link to some study abstracts that provides additional details. Please note that this is not a comprehensive list of all SV40-associated cancers or all medical/scientific articles written about the detection of SV40 in cancer.


Brain Cancers

Astrocytoma
Anaplastic Astrocytoma
Choroid Plexus Papilloma
Ependymoma
Gemistocytic Astrocytoma
Glioblastoma
Gliosarcoma
Medulloblastoma
Meningioma
Oligodendroglioma
Pituitary Adenoma
 
Bone Cancers

Osteosarcoma
Ewing’s Tumors
 
Chest Cancers

Mesothelioma
 
Lymphomas

Non-Hodgkins Lymphoma (NHL)
 
Thyroid Cancers

Papillary thyroid carcinomas
Anaplastic thyroid carcinomas (ATC)
 
 

[larsonstdoc]

http://www.naturalnews.com/032854_SV40_polio_vaccines.html

   more at the link.....


The true story of SV40, the cancer-causing virus hidden in polio vaccines


(NaturalNews) Poliomylitis, or polio for short, is a disease that has been around since ancient times, and despite the medical advances we have made in the United States in terms of regular and natural health, there is still no cure for this dreaded, disabling disease.

An infectious viral affliction that attacks nerve cells and, at times, the body's central nervous system, polio causes a phenomenon known as muscle wasting (a decrease in the mass of muscle), and can also cause paralysis and death.

"Since 1900 there had been cycles of epidemics, each seeming to get stronger and more disastrous. The disease, whose early symptoms are like the flu, struck mostly children, although adults, including Franklin Roosevelt, caught it too," said a report in the journal A Science Odyssey.

In 1952 that all changed, when Dr. Jonas Salk, a medical student and virus researcher, developed a vaccine against polio that, two years later, was accepted for testing nationwide. The principle behind the vaccine was simple and familiar: Like the vaccine that had been developed to fight smallpox, the polio vaccine introduced a small amount of the virus into the body, which then developed antibodies and an ability to fight off more powerful strains of the disease.

Admittedly, Salk's vaccine logged early success; some 60-70 percent of those vaccinated did not develop the disease. But it also saw some early problems. About 200 people who had been vaccinated got the disease, and 11 of them died, forcing a halt to all testing. Once it was determined that a faulty, poorly manufactured batch of the vaccine was the cause of those cases, stricter production standards were implemented and full-scale vaccinations nationwide resumed once more. Four million vaccines were given by 1955; by 1959, 90 countries were using it.

That said, those early cases were far from the last time the vaccine killed. In fact, throughout its history of use, Salk's polio vaccine left a path of death its wake.

A deadly discovery

Production and nationwide distribution of the polio vaccine was in full force by the end of the 1950s, but between 1959 and 1960 Dr. Bernice Eddy, a researcher with the National Institute of Health (NIH), made a startling discovery.

While examining the minced kidney cells of rhesus monkeys - from which the the polio vaccines were derived - she discovered "that the cells would die without any apparent cause," according to a report by Michael E. Horwin, M.A., J.D., published in the Nov. 3, 2003, issue of the Albany Law Journal of Science & Technology.

Horwin writes:

Dr. Eddy discovered that the cells would die without any apparent cause. She then took suspensions of the cellular material from these kidney cell cultures and injected them into hamsters. Cancers grew in the hamsters. Shortly thereafter, scientists at the pharmaceutical company Merck & Co. discovered what would later be determined to be the same virus identified by Eddy. This virus was named Simian Virus 40 or SV40 because it was the 40th simian virus found in monkey kidney cells.

[jofortruth]

Excerpts from a book entitled "The Health Century" by a Canadian Dr. Edward Shorter which backs up how Merck and buddies hid the cancer virus in their vaccines in the 1950s. Dr Eddy was a hero back then in exposing this fraud, and IMO was murdered by operatives of the big pharma cartel who didn't want her info exposed any further. Read Dr. Mary's Monkey and you will see the story told that confirms this book and tells of her murder): (I have a copy of the book, so these excerpts are verbatim of the books pages they signify):
http://www.whale.to/v/eddy.html

Dr Mary's Monkey is A MUST READ:
http://z4.invisionfree.com/The_Great_Deception/index.php?showtopic=7017

[TahoeBlue]

most important take of previous posts is that SV40 is in the population even now and is passed on like hiv or hepatitis - No studies are public because they don't want people to know! At least 10 percent of the population has SV40 ...

http://www.biomedcentral.com/content/pdf/1750-9378-2-13.pdf
Simian virus 40 in humans
...
 To date, the prevalence of SV40 infections in humans is not known. Recent studies, based on PCR and serological techniques, indicate that SV40 infection occurs both in children and adults.

(i) SV40 DNA sequences have been detected in normal and neoplastic tissues of people either too young (1 to 30 years) or too old (60 to 85 years) to have been vaccinated with SV40-contaminated anti-polio vaccines [19,33,76-81].

This finding may also explain the lack of difference in cancer incidence between individuals vaccinated with SV40-contaminated and SV40-free anti-polio vaccines
...

http://www.ncbi.nlm.nih.gov/pubmed/23621738
Mikrobiyol Bul. 2013 Apr ;47(2):362-81.
...
In addition SV40 seropositivity was reported in human populations although in low rates (2-10%). 

These data have raised the possibility that SV40 infects humans and circulates in human populations unrelated to being exposed to the vaccine.

[TahoeBlue]

http://cmr.asm.org/content/17/3/495/T1.expansion
Emergent Human Pathogen Simian Virus 40 and Its Role in Cancer

TABLE 1.
SV40 seropositivity of hospitalized children in Houston, Tex.a

Populationcharacteristic

No. SV40 seropositiveb/no. of patients (% seropositive)

age:  (percent) 
 10-15 14/154 (9.1)
 ...

↵a From reference 12, used with permission.
↵b Seropositivity was determined by using an SV40-specific plaque reduction neutralization assay in tissue culture cells.

↵c There was a significant association of SV40 seropositivity with kidney transplantation (6 of 15 [40.0%]) compared to other diagnoses (8 of 238 [3.4%]) (P < 0.001).

[jofortruth]

(Continued from post above where you can find the pdfs of these excerpts) Excerpts from "The Health Century" by Dr Edward Shorter (pgs  195, 196, 201, 203)










See also the video "In Lies We Trust - The CIA, Hollywood & Bioterrorism" (Starting time 32:00 approx where Dr. Hilleman audio of interview. The pgs above are the same as the audio of Hilleman)
https://www.youtube.com/watch?v=NkHcEGZ8oVs

THERE IS A DISHONESTY, OR WORSE, IMO, IN BIG PHARMA AND THE MEDICAL INDUSTRY, AND IT GOES WAY BACK AS SHOWN BY THIS MATERIAL! NOTHING WILL CHANGE UNTIL THE FILTH AT THE TOP IS DEALT WITH AND THEY ARE HELD ACCOUNTABLE FOR THEIR CRIMES AGAINST HUMANITY!

[jofortruth]

Another page showing coverup by Merck:

[John_Back_From_The_Club_O]

http://www.thelibertybeacon.com/2013/07/12/cdc-admits-as-many-as-30-million-americans-could-be-at-risk-for-cancer-due-to-polio-vaccine/

Do vaccines cause cancer? Well Straight from the horses mouth, The CDC says it just may be so … but after 50 years they state more studies are needed (REALLY?).

The Centers for Disease Control and Prevention (CDC) posts on its own website the concern that as many as 30 million Americans could be at risk for cancer after receiving a Polio vaccination during the 1955 – 1963 time frame. This possibility exists because the vaccine in question was found to be contaminated with the SV40 virus. Most Americans received multiple doses of this vaccine that was administered to almost 100 million people.

It is stated that after the discovery (in 1960), any newly manufactured Polio vaccine was free of this virus (it took 3 years). No information is available as to exactly how much of the vaccine was tainted at the time, nor is there any information as to the controls put in place to insure all the tainted vaccine was effectively recalled.

vaccination during the 1955 – 1963 time frame
It doesn't take much research to figure out that the generation that received the 1955- 1963 polio vaccine were the MOST cancer stricken generation up to that time.

To cover their tracks the meme was put out THAT PEOPLE IN THE PAST DID NOT LIVE AS LONG.  You really have to be an uneducated moron to fall for this lie.  The average age of this cancer ridden generation was around 48 years old when the got diagnosed with their cancer.  I can go to ANY cemetery and read the tombstones and SEE that people lived much longer then 48 years old for God sake!

In the 'Physicians Desk Reference and in vaccine inserts it is stated in black and white that NO vaccine is tested for carcinogens.

Now, how many pediatricians actually tell their victims err, I mean, patients this information?

... and now the drug companies are just boldly stating that they intend to use actual cancer tumor cells in vaccines.   Which begs the question what other hazardous material are the... offshore... can't be taken to a court of law drug company's going to spike their poison vaccines with. 

[TahoeBlue]

vaccination during the 1955 – 1963 time frame
It doesn't take much research to figure out that the generation that received the 1955- 1963 polio vaccine were the MOST cancer stricken generation up to that time.

To cover their tracks the meme was put out THAT PEOPLE IN THE PAST DID NOT LIVE AS LONG.  You really have to be an uneducated moron to fall for this lie.  The average age of this cancer ridden generation was around 48 years old when the got diagnosed with their cancer.  I can go to ANY cemetery and read the tombstones and SEE that people lived much longer then 48 years old for God sake!

...

What I have shown in this any other threads is that SV40 IS NOW IN THE POPULATION WITHOUT VACCINES - we pass it along the Hepatitis or HIV  and the Govt. refuses to create tests for sv40 or do studies as to who has it ... the studies that is does accept are the ones that attempt to show that SV40 does not cause cancer.... ... or acknowledge that it is out in the wild KILLING PEOPLE ...   

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC452549/

Clin Microbiol Rev. Jul 2004; 17(3): 495–508.
doi:  10.1128/CMR.17.3.495-508.2004
PMCID: PMC452549
Emergent Human Pathogen Simian Virus 40 and Its Role in Cancer
Regis A. Vilchez1,2 and Janet S. Butel2,*
Author information ► Copyright and License information ►

...
Therefore, as SV40 is recognized as a potent oncogenic agent, it is important to evaluate the increasing data that implicate the virus in some human malignancies. This review examines the biological, pathological and clinical evidence of SV40 pathogenesis and discusses future directions needed to define an etiologic role for the virus in some of these devastating diseases.
...
 Infectious SV40 survived the vaccine inactivation treatments, and conservative estimates indicate that up to 30 million people (children and adults) in the United States may have been exposed to live SV40 from 1955 through 1963 when administered potentially contaminated polio vaccines (95, 111).

Millions of people worldwide were also potentially exposed to SV40 because contaminated polio vaccines were distributed and used in many countries (85, 123). These data led the Institute of Medicine to conclude that “the biological evidence is of moderate strength that SV40 exposure from the polio vaccine is related to SV40 infection in humans” (111).

https://www.einstein.yu.edu/uploadedFiles/EJBM/SV40_Cancer_14-20.pdf
Einstein Quarterly Journal of Biology and Medicine (2001) 18:14-20
Simian Virus 40 (SV40) and Human Cancers
...
Evidence is mixed, though, regarding the detection of SV40 infection in the general population.
Several studies have also failed to detect the virus in human tumors. Even among the positive studies, there are
inconsistencies regarding the prevalence of SV40 DNA in normal tissues, and the very low levels of virus detected in tumors
suggests that only a fraction of tumor cells probably contain viral sequences. An aggressive campaign to study the role of
SV40 in human disease has been initiated, and despite the current uncertainties, it will almost certainly be known within the
next few years whether SV40 is a human tumor virus .


http://jvi.asm.org/content/77/9/5039.full
Simian Virus 40 Infection of Humans

Robert L. Garcea1 and
 Michael J. Imperiale2,*
 
J. Virol. May 2003   vol. 77  no. 9  5039-5045

What is needed to enhance our understanding of SV40 infection in humans and the role of SV40 in human malignancies? Current data on SV40 replication and transmission in human populations are nearly uninterpretable and will not improve until a highly specific serological assay for SV40 is used to analyze clinical samples.

Such an immunoassay has been difficult to devise because of extensive cross-reactivity of the SV40 capsid proteins with those of BKV and JCV. Virus neutralization assays are extremely labor-intensive and have not been directly compared among the viruses. Recently, however, recombinant VP1 capsid proteins for SV40, JCV, and BKV have been prepared as virus-like particle preparations for use in enzyme-linked immunosorbent assays (K. Shah and D. Galloway, personal communications). The initial serological studies using these reagents have not detected specific or robust SV40 immune responses in any samples tested. A small fraction (5 to 7%) of sera (K. Shah, personal communication) have low-level reactivity with SV40 VP1 that may be due to cross-reactivity with JCV or BKV VP1 or to a transient SV40 infection. These assays will now permit case-controlled studies, however, comparing individuals with SV40-associated malignancies to control populations.
...
At this time, some members of the jury remain undecided about a role for SV40 in human disease. Seroepidemiology and a basic understanding of virus biology in humans are essential pieces missing from the puzzle. Perhaps we expect SV40 to follow the “rules” for other oncogenic viruses such as human papillomavirus and Epstein-Barr virus. Rather, SV40 may be generating novel rules, leading the way as it has before into new paradigms of virus biology and pathogenesis.

[John_Back_From_The_Club_O]

What I have shown in this any other threads is that SV40 IS NOW IN THE POPULATION WITHOUT VACCINES - we pass it along the Hepatitis or HIV  and the Govt. refuses to create tests for sv40 or do studies as to who has it ... the studies that is does accept are the ones that attempt to show that SV40 does not cause cancer.... ... or acknowledge that it is out in the wild KILLING PEOPLE ...   

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC452549/

Clin Microbiol Rev. Jul 2004; 17(3): 495–508.
doi:  10.1128/CMR.17.3.495-508.2004
PMCID: PMC452549
Emergent Human Pathogen Simian Virus 40 and Its Role in Cancer
Regis A. Vilchez1,2 and Janet S. Butel2,*
Author information ► Copyright and License information ►

...
Therefore, as SV40 is recognized as a potent oncogenic agent, it is important to evaluate the increasing data that implicate the virus in some human malignancies. This review examines the biological, pathological and clinical evidence of SV40 pathogenesis and discusses future directions needed to define an etiologic role for the virus in some of these devastating diseases.
...
 Infectious SV40 survived the vaccine inactivation treatments, and conservative estimates indicate that up to 30 million people (children and adults) in the United States may have been exposed to live SV40 from 1955 through 1963 when administered potentially contaminated polio vaccines (95, 111).

Millions of people worldwide were also potentially exposed to SV40 because contaminated polio vaccines were distributed and used in many countries (85, 123). These data led the Institute of Medicine to conclude that “the biological evidence is of moderate strength that SV40 exposure from the polio vaccine is related to SV40 infection in humans” (111).

https://www.einstein.yu.edu/uploadedFiles/EJBM/SV40_Cancer_14-20.pdf
Einstein Quarterly Journal of Biology and Medicine (2001) 18:14-20
Simian Virus 40 (SV40) and Human Cancers
...
Evidence is mixed, though, regarding the detection of SV40 infection in the general population.
Several studies have also failed to detect the virus in human tumors. Even among the positive studies, there are
inconsistencies regarding the prevalence of SV40 DNA in normal tissues, and the very low levels of virus detected in tumors
suggests that only a fraction of tumor cells probably contain viral sequences. An aggressive campaign to study the role of
SV40 in human disease has been initiated, and despite the current uncertainties, it will almost certainly be known within the
next few years whether SV40 is a human tumor virus .


http://jvi.asm.org/content/77/9/5039.full
Simian Virus 40 Infection of Humans

Robert L. Garcea1 and
 Michael J. Imperiale2,*
 
J. Virol. May 2003   vol. 77  no. 9  5039-5045

What is needed to enhance our understanding of SV40 infection in humans and the role of SV40 in human malignancies? Current data on SV40 replication and transmission in human populations are nearly uninterpretable and will not improve until a highly specific serological assay for SV40 is used to analyze clinical samples.

Such an immunoassay has been difficult to devise because of extensive cross-reactivity of the SV40 capsid proteins with those of BKV and JCV. Virus neutralization assays are extremely labor-intensive and have not been directly compared among the viruses. Recently, however, recombinant VP1 capsid proteins for SV40, JCV, and BKV have been prepared as virus-like particle preparations for use in enzyme-linked immunosorbent assays (K. Shah and D. Galloway, personal communications). The initial serological studies using these reagents have not detected specific or robust SV40 immune responses in any samples tested. A small fraction (5 to 7%) of sera (K. Shah, personal communication) have low-level reactivity with SV40 VP1 that may be due to cross-reactivity with JCV or BKV VP1 or to a transient SV40 infection. These assays will now permit case-controlled studies, however, comparing individuals with SV40-associated malignancies to control populations.
...
At this time, some members of the jury remain undecided about a role for SV40 in human disease. Seroepidemiology and a basic understanding of virus biology in humans are essential pieces missing from the puzzle. Perhaps we expect SV40 to follow the “rules” for other oncogenic viruses such as human papillomavirus and Epstein-Barr virus. Rather, SV40 may be generating novel rules, leading the way as it has before into new paradigms of virus biology and pathogenesis.

Yes, Yes!  This is highly accurate.

If lab created monkey viruses are being passed generation to generation from the 1950's what kind of viruses from today's vaccines are we passing on to future generations of humans on planet earth?  The sky is literally the limit.

[TahoeBlue]

Just found this one:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2375249/
Br J Cancer. 2001 Nov; 85(9): 1295–1297.
Published online 2001 Sep 1. doi:  10.1054/bjoc.2001.2065
PMCID: PMC2375249
Thirty-five year mortality following receipt of SV40- contaminated polio vaccine during the neonatal period
C Carroll-Pankhurst,1 E A Engels,2 H D Strickler,2 J J Goedert,2 J Wagner,3 and E A Mortimer Jr3

Abstract

Early poliovirus vaccines, both inactivated and live attenuated, were inadvertently contaminated with simian virus 40 (SV40), a monkey virus known to be oncogenic for newborn hamsters. Although large epidemiologic studies have not identified an elevated cancer risk in persons who received SV40-contaminated vaccines, fragments of SV40 DNA have recently been identified in certain human tumours.

We report the follow-up of a cohort of 1073 persons, unique because they received SV40-contaminated poliovirus vaccines as newborns in 1961–63. A previous report of the status of these subjects as of 1977–79 identified 15 deaths, none due to cancer.

The present study utilized the National Death Index to identify deaths in the cohort for the years 1979–96. Expected deaths were calculated from Cleveland area sex-, age-, race- and year-specific mortality rates. Increased mortality from all causes was not found. 4 deaths from cancer were found compared to 3.16 expected (P= 0.77). However, 2 deaths from testicular cancer occurred, compared to 0.05 expected (P= 0.002), which may be a chance finding due to multiple comparisons. There were 2 deaths due to leukaemia, a non-significant finding, and no deaths due to tumours of the types putatively associated with SV40. Although these results are, for the most part, consistent with other negative epidemiologic investigations of risks from SV40-contaminated vaccines, further study of testicular cancer may be warranted, and it will be important to continue monitoring this cohort which is now reaching middle-age. © 2001 Cancer Research Campaign

see: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC452549/

http://jnci.oxfordjournals.org/content/95/1/38
Trends in U.S. Pleural Mesothelioma Incidence Rates Following Simian Virus 40 Contamination of Early Poliovirus Vaccines
Received April 5, 2002

Abstract

Background: Poliovirus vaccines that were used during the late 1950s and early 1960s were contaminated with simian virus 40 (SV40), a monkey virus that is tumorigenic in rodents. SV40 DNA sequences have been detected in some human cancers, especially pleural mesotheliomas, although results are conflicting. We examined the relationship between SV40-contaminated poliovirus vaccine exposure and subsequent rates of pleural mesothelioma in the United States. Methods: We used data from the Surveillance, Epidemiology, and End Results Program to estimate age- and sex-specific pleural mesothelioma incidence rates per 105 person-years (py) from 1975 through 1997 and the Poisson distribution to determine 95% confidence intervals (CIs) for each rate. The prevalence, by birth cohort, of poliovirus vaccine exposure during the period of widespread SV40 contamination was determined from published survey data. Trends in mesothelioma incidence rates were assessed by examining age- and sex-specific rates over calendar periods and with the use of the age–period–cohort model. Trends in mesothelioma incidence were then compared with trends in prevalence of exposure. All statistical tests were two-sided. Results: The age-standardized pleural mesothelioma incidence rate for 1975 through 1997 was 1.29/105 py (95% CI = 1.24/105 to 1.34/105 py) in males and 0.21/105 py (95% CI = 0.20/105 to 0.23/105 py) in females. The rate in males increased from 0.79/105 py (95% CI = 0.62/105 to 1.0/105 py) in 1975 to a peak of 1.69/105 py (95% CI = 1.46/105 to 1.95/105 py) in 1992. Incidence rates increased the most among males who were 75 years of age or older, the age group least likely to have been immunized against poliovirus. Incidence rates among males in the age groups most heavily exposed to SV40-contaminated poliovirus vaccine remained stable or decreased from 1975 through 1997. Similar age-specific trends were observed among females. The age–period–cohort models for men and women also indicated that the trends in pleural mesothelioma incidence were not related to trends in exposure to SV40-contaminated poliovirus vaccine. Conclusions: Age-specific trends in U.S. pleural mesothelioma incidence rates are not consistent with an effect of exposure to SV40-contaminated poliovirus vaccine. Nonetheless, given reports of the detection of SV40 genomic DNA sequences in human mesotheliomas, monitoring of vaccine-exposed cohorts should continue.

http://www.ncbi.nlm.nih.gov/books/NBK221112/
Immunization Safety Review: SV40 Contamination of Polio Vaccine and Cancer.

...

For its evaluation of the hypothesis on SV40-contaminated polio vaccine and cancer, the committee held an open scientific meeting in July 2002 (see Appendix B) to hear presentations on issues germane to the topic. The presentations to the committee at the open meeting are available in electronic form (audio files and slides) on the project website (www.iom.edu/imsafety). In addition, the committee reviewed an extensive collection of material, primarily from the published, peer-reviewed scientific and medical literature. A list of the materials reviewed by the committee, including many items not cited in this report, can be found on the project's website.

...

Despite its great value in controlling a devastating disease, polio vaccine is a source of concern because at least some of the vaccines used between 1955 and 1963, when more than 98 million persons were vaccinated in the United States, are known to have been contaminated with SV40.

SV40 is a polyomavirus that commonly infects certain species of Asian macaques, especially the rhesus monkey. Other polyomaviruses, which are generally species-specific, include the BK and JC viruses of humans. Polyomaviruses are a genus of the papovavirus family of DNA viruses. This family also includes the papillomaviruses, of which one—human papillomavirus (HPV)—is causally associated with cervical cancer.
...

IPV administered between 1955 and 1963 to about 98 million children and adults is assumed to be the primary source of human exposure to SV40 in the United States.4 In addition, experimental lots of OPV contaminated with SV40 was administered to about 10,000 people participating in clinical trials between 1959 and 1961. Recipients of the oral vaccine, in contrast to those receiving contaminated IPV, did not develop an antibody response to SV40 (as reviewed in Shah and Nathanson, 1976). This suggests that IPV, not OPV, resulted in the infection of humans with SV40. Nonetheless, concerns about the validity, and in particular the specificity for SV40, of the serologic testing create some uncertainty about this conclusion.
...

Studies of groups of people who received polio vaccine during 1955–1963 provide evidence of no increased cancer risk.

However, because these epidemiologic studies are sufficiently flawed, the Institute of Medicine's Immunization Safety Review Committee concluded that the evidence was inadequate to conclude whether or not the contaminated polio vaccine caused cancer. In light of the biological evidence supporting the theory that SV40-contamination of polio vaccines could contribute to human cancers, the committee recommends continued public health attention in the form of policy analysis, communication, and targeted biological research. Box 3 summarizes the committee's conclusions and recommendations.

[Due_Process_NonNegotiable]

Any info from an actual CDC source?

[TahoeBlue]

Any info from an actual CDC source?

They continue to bury this story and promote screwed up studies ...

But a lot of the sources in this thread is the NIH ie the national institute of health - the source of info for the cdc OK?
http://www.nih.gov/about/
,.,,
NIH is the largest source of funding for medical research in the world, creating hundreds of thousands of high-quality jobs by funding thousands of scientists in universities and research institutions in every state across America and around the globe.


[ This page Just recently removed !!!! :]    try the link I just used a few days ago !!!

http://www.cdc.gov/vaccinesafety/updates/archive/polio_and_cancer_factsheet.htm
Cancer, Simian Virus 40 (SV40), and Polio Vaccine Fact Sheet
...

Q: Can I be tested for SV40?

A: An accurate blood test does not exist. Current antibody blood tests can be inaccurate, scientists say, because they also may detect the presence of closely related viruses, and SV40 may be present at such a low level that no antibodies are produced. Researchers are working to create an effective test.

http://www.medicaldaily.com/cdc-removes-webpage-about-polio-vaccine-contamination-further-admission-guilt-249339
CDC Removes Webpage About Polio Vaccine Contamination: Further Admission Of Guilt?

Aug 6, 2013 02:36 PM  By Susan Scutti
The Centers for Disease Control and Prevention reportedly removed a webpage about polio vaccine contamination from its site.   USGov-HHS-CDC

....

A few days ago, Natural News reported that the Centers for Disease Control and Prevention (CDC) had removed from its website an official fact sheet — entitled Cancer Simian Virus 40 (SV40), and Polio Vaccine — that explained the history of this public health error. Today, if you search that article, which provides a link to an archived fact sheet, you will be led down a cold trail. At another website, Above Top Secret, you will find similar claims with cut-and-pasted archival materials as well as the observation that this contamination issue had been documented in many places and the CDC's webpage is hardly a revelation. (The comment section, though, is worth reading and provides many points of view on the actions of the CDC.)

Where does this leave us?

Arguments have been made that the incidence of childhood cancer has risen since the 1960s. According to the American Childhood Cancer Organization, about one in 300 boys and one in 333 girls will develop cancer before their 20th birthday. The organization also states that there was an 118-percent increase in incidence among 0- to 19-year-olds between the years 1975 and 2006. According to Horwin, SV40 has been implicated in a variety of human cancers, including those affecting the brain, bone, and lungs. "[Scientists from around the world] have found SV40 antibodies in a significant percentage of people including children who were too young to receive the SV40 contaminated vaccines of the early 1960's," stated Horwin.


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http://wwwnc.cdc.gov/eid/article/3/2/97-0227_article

Volume 3, Number 2—June 1997

News and Notes

Simian Virus 40 (SV40), a Possible Human Polyomavirus (Workshop Held at NIH)

[TahoeBlue]

Here's another NIH article from 2004 :

http://www.ncbi.nlm.nih.gov/pubmed/15015494
Virology. 2004 Jan 5;318(1):1-9.
Simian virus 40 infection in humans and association with human diseases: results and hypotheses.
Barbanti-Brodano G1, Sabbioni S, Martini F, Negrini M, Corallini A, Tognon M.

Author information 1Department of Experimental and Diagnostic Medicine, Section of Microbiology, Center of Biotechnology, University of Ferrara, I-44100, Ferrara, Italy

Abstract

Simian virus 40 (SV40) is a monkey virus that was introduced in the human population by contaminated poliovaccines, produced in SV40-infected monkey cells, between 1955 and 1963.
Epidemiological evidence now suggests that SV40 may be contagiously transmitted in humans by horizontal infection, independent of the earlier administration of SV40-contaminated poliovaccines.
This evidence includes detection of SV40 DNA sequences in human tissues and of SV40 antibodies in human sera, as well as rescue of infectious SV40 from a human tumor.

Detection of SV40 DNA sequences in blood and sperm and of SV40 virions in sewage points to the hematic, sexual, and orofecal routes as means of virus transmission in humans. The site of latent infection in humans is not known, but the presence of SV40 in urine suggests the kidney as a possible site of latency, as it occurs in the natural monkey host.

SV40 in humans is associated with inflammatory kidney diseases and with specific tumor types: mesothelioma, lymphoma, brain, and bone.

These human tumors correspond to the neoplasms that are induced by SV40 experimental inoculation in rodents and by generation of transgenic mice with the SV40 early region gene directed by its own early promoter-enhancer. The mechanisms of SV40 tumorigenesis in humans are related to the properties of the two viral oncoproteins, the large T antigen (Tag) and the small t antigen (tag). Tag acts mainly by blocking the functions of p53 and RB tumor suppressor proteins, as well as by inducing chromosomal aberrations in the host cell. These chromosome alterations may hit genes important in oncogenesis and generate genetic instability in tumor cells. The clastogenic activity of Tag, which fixes the chromosome damage in the infected cells, may explain the low viral load in SV40-positive human tumors and the observation that Tag is expressed only in a fraction of tumor cells. "Hit and run" seems the most plausible mechanism to support this situation. The small tag, like large Tag, displays several functions, but its principal role in transformation is to bind the protein phosphatase PP2A. This leads to constitutive activation of the Wnt pathway, resulting in continuous cell proliferation.

The possibility that SV40 is implicated as a cofactor in the etiology of some human tumors has stimulated the preparation of a vaccine against the large Tag. Such a vaccine may represent in the future a useful immunoprophylactic and immunotherapeutic intervention against human tumors associated with SV40.

[TahoeBlue]

Still checking this out - seems to be new  - an SV40 foundation .org

http://www.sv40foundation.org/Who-we-are.html

This foundation was created by Raphaele and Michael Horwin, parents of Alexander Horwin. Alexander was born on June 7, 1996. He was administered the oral polio vaccine in November 1997. On August 10, 1998, Alexander was diagnosed with a malignant brain cancer, medulloblastoma. Alexander died on January 31, 1999.

Four independent laboratories (Baylor College of Medicine, University of Chicago, University of Texas Southwestern Medical Center, Temple University) used DNA testing (Polymerase Chain Reaction (PCR)) or laser micro-dissection to test Alexander’s tumor for the presence of SV40. Every lab found that the tumor tissue contained the virus.

In addition, Alexander’s cord blood was saved and stored by a private laboratory. The cord blood was the blood shared by Alexander and his mother at the time of Alexander's birth. This blood was tested for SV40 using PCR. It did not contain SV40.

Alexander’s parents were tested for SV40 by two independent laboratories (Baylor College of Medicine, University of Wales) using a number of PCR tests. All tests demonstrated that the parents did not carry the virus.

A website in memory of Alexander is available at: www.ouralexander.org

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http://www.sv40foundation.org/Demanding-CI.html

Demanding a Congressional Investigation into SV40

On June 7, 2003 we wrote a letter to Congressman Dan Burton, Chair of the Subcommittee on Human Rights and Wellness, U.S. Government Reform Committee in which we suggested that a Congressional Hearing be held to initiate investigations into SV40 and the public health.  A few weeks later, Congressman Burton called us by telephone and we discussed the issue at length.  We emphasized the importance of having a hearing in which the leading scientific experts would testify followed by parents who have lost children to SV40 positive cancers.  Mr. Burton agreed with this approach and decided to schedule the hearing.  He asked us to testify, to provide a list of scientists and parents, and to facilitate their participation.

| - - - -

http://www.ouralexander.org/
....
About Childhood Vaccinations and  Simian Virus 40 (SV40)

Request for Congressional Investigation: (MS Word document) June 7, 2003 Letter to The Honorable Dan Burton, Chairman of the House Government Reform Subcommittee on Human Right and Wellness, to Demand a Congressional Investigation and Hearing on the Introduction of Simian Virus 40 (SV40), a Cancer-Causing Monkey Virus, into the American Population From Contaminated Polio Vaccines

State of the Vaccine Nation: One hundred years ago, children received one vaccine. Forty years ago, children got five vaccines routinely by two years of age. Children now receive 52 vaccines, in the form of 15 shots, by the time they are six months of age if they receive all the recommend shots. Vaccines contain mercury, which has been associated with neurological disorders in children including ADD learning difficulties, Autism and speech delays.

[TahoeBlue]

geez sv40 in east European  oral polio vaccines after 1961 up til 1978 !!! :

http://cancerres.aacrjournals.org/content/65/22/10273.full
Cancer Res November 15, 2005   65;  10273 

Some Oral Poliovirus Vaccines Were Contaminated with Infectious SV40 after 1961

Rochelle Cutrone1,
 John Lednicky3,
 Glynis Dunn4,
 Paola Rizzo2,
 Maurizio Bocchetta1,
 Konstantin Chumakov5,
 Philip Minor4, and
 Michele Carbone1
 

+
 Author Affiliations
1Thoracic Oncology Program and 2Breast Cancer Program, Cardinal Bernardin Cancer Center, and 3Laboratory of Virology, Department of Pathology, Loyola University, Chicago, Illinois; 4National Institute for Biological Standards and Control, Herts, United Kingdom; and 5Food and Drug Administration, Rockville, Maryland 
Requests for reprints:
 Michele Carbone, Thoracic Oncology Program, Cardinal Bernardin Cancer Center, Loyola University Chicago Medical Center, Room 205, 2160 South First Avenue, Maywood, IL 60153. Phone: 708-327-3250; Fax: 708-327-3238; E-mail: [email protected].


Abstract

Some polio vaccines prepared from 1954 to 1961 were contaminated with infectious SV40. It has been assumed that all polio vaccines were SV40 free in the United States after 1961 and in other countries after 1962.

Following a WHO requirement that was prompted by the detection of SV40 in some human tumors, we conducted a multilaboratory study to test for SV40 polio vaccines prepared after 1961. Vaccine samples from 13 countries and the WHO seed were initially tested by PCR. The possible presence of intact and/or infectious SV40 DNA in PCR-positive samples was tested by transfection and infection of permissive CV-1 cells. All results were verified by immunohistochemistry, cloning, and sequencing.

All the vaccines were SV40 free, except for vaccines from a major eastern European manufacturer that contained infectious SV40. We determined that the procedure used by this manufacturer to inactivate SV40 in oral poliovirus vaccine seed stocks based on heat inactivation in the presence of MgCl2 did not completely inactivate SV40.

These SV40-contaminated vaccines were produced from early 1960s to about 1978 and were used throughout the world. Our findings underscore the potential risks of using primary monkey cells for preparing poliovirus vaccines, because of the possible contamination with SV40 or other monkey viruses, and emphasize the importance of using well-characterized cell substrates that are free from adventitious agents. Moreover, our results indicate possible geographic differences in SV40 exposure and offer a possible explanation for the different percentage of SV40-positive tumors detected in some laboratories.


Introduction:

Inactivated poliovirus vaccine (IPV) and live oral poliovirus vaccines (OPV) were prepared in primary cell cultures derived from rhesus monkey kidneys. Studies of these vaccines led to the discovery of a new virus called SV40 in 1959. This DNA virus caused vacuolization of green monkey cell cultures and was found to be highly oncogenic in hamsters (reviewed in refs. 1, 2). It was found that SV40 was endemic in rhesus monkeys. For this reason, the rhesus kidney cell cultures used to manufacture poliovirus vaccines as well as some seed stocks of poliovirus contained infectious SV40 ( 2– 5). Therefore, the early batches of OPV contained infectious SV40 ( 3– 5). Because formaldehyde treatment used to prepare IPV failed to completely inactivate SV40, some batches of IPV contained infectious SV40 ( 2, 4). As a result, it has been estimated that >100 million people in the United States and many more worldwide received potentially contaminated vaccines prepared during the years 1954 to 1961 ( 2).

Regulations adopted in 1961 required new batches of poliovirus vaccines prepared in the United States to be free of SV40  [ They KNEW!!! ] and it has been assumed that they were based on quality-control testing done during vaccine manufacture (documents concerning the contamination of polio vaccines with SV40 and the history of polio vaccination can be found in the text and appendices to ref. 4). In the United States, OPV was licensed after SV40 was discovered; therefore, these vaccines should have been free from SV40

,...

Tests to identify the cause of the residual SV40 contamination in eastern European vaccine manufacturer oral poliovirus vaccines. We asked why SV40 was still present in the EEVM vaccines but had been successfully removed from the UK vaccines. The EEVM received its seed stocks from Dr. Sabin in the late 1950s. These stocks were later found to be contaminated with 105 pfu/mL SV40 ( 5). Moreover, ∼47% of the rhesus monkeys used to prepare polio vaccines were infected with SV40 ( 5).

In 1962, the EEVM switched to primary African green monkey cells that were supposedly SV40 free, and rigorous quality-control measures to test for the presence of SV40 in these monkeys were implemented ( 5). In addition, Sabin poliovirus stocks were treated with a procedure proposed in 1961 ( 16) to remove live SV40 ( 5). The procedure involved thermal inactivation of SV40 under conditions where poliovirus was selectively protected by the addition of 1 mol/L MgCl2.
...

Our results indicate that heat inactivation in the presence of MgCl2 failed to completely inactivate SV40 in poliovirus seed stocks
...

A recent seroprevalence study of SV40 infection in Kazakhstan, which is in the geographic area of distribution of the contaminated EEVM vaccines, reported that 60% of the subjects seropositive for SV40 were born from 1960 to 1980s ( 29). The authors of this report noted that this was “a time period in which the vaccines should have been expected to be free of SV40 ( 29).” Our results provide a possible explanation for these findings because it is possible that the vaccines distributed in Kazakhstan from 1960 to 1980 were not SV40 free.
...

[TahoeBlue]

bump recreated

[TahoeBlue]

It's interesting they put a damper on studies after 2002 or so ...

http://jasn.asnjournals.org/content/13/9/2320.full
Molecular Identification of SV40 Infection in Human Subjects and Possible Association with Kidney Disease

Rui-Mei Li*,
 Mary H. Branton*,
 Somsak Tanawattanacharoen*,
 Ronald A. Falk†,
 J. Charles Jennette† and
 Jeffrey B. Kopp*


Abstract

ABSTRACT. Simian virus 40 (SV40), a monkey polyomavirus that is believed to have entered the human population through contaminated vaccines, is known to be renotropic in simians. If indeed SV40 is endemic within the human population, the route of transmission is unknown. It was therefore hypothesized that SV40 might be renotropic in humans and be detected more frequently in samples obtained from patients with kidney diseases.

This study found that typical polyomavirus cytopathic effects (CPE) were present and SV40 T antigen was detected in CV-1 cells cultured with peripheral blood mononuclear cells (PBMC) or urinary cells obtained from patients with kidney disease and healthy volunteers. DNA sequences homologous to the SV40 viral regulatory genome were detected by PCR in urinary cells from 15 (41%) of 36 patients with focal segmental glomerulosclerosis (FSGS), 2 (10%) of 20 patients with other kidney diseases, and 1 (4%) of 22 healthy volunteers (FSGS compared with other glomerular disease, P < 0.02; FSGS compared with healthy volunteers, P = 0.003).

SV40 viral regulatory region genome was detected from PBMC at similar frequencies in patients with FSGS (35%), other glomerular diseases (20%), and healthy volunteers (22%). SV40 genome was detected by PCR in kidney tissues from 17 (56%) of 30 of patients with FSGS and 4 (20%) of 20 patients with minimal change disease and membranous nephropathy (P < 0.01). Considerable genetic heterogeneity of the viral regulatory region was detected, which argues against laboratory contamination. SV40 genome was localized to renal tubular epithelial cell nuclei in renal biopsies of patients with FSGS by in situ hybridization.

This study demonstrates for the first time that human kidney can serve as a reservoir for SV40 replication and that SV40 may contribute to the pathogenesis of kidney disease, particularly FSGS.


SV40, a monkey polyomavirus, was present in poliovaccines and adenovirus vaccines used between 1955 and 1963, and it is believed to have been introduced into the human population at that time (1,2). Several lines of evidence suggest that new SV40 infections may be occurring in the human population.

David et al. (3) found that 16% peripheral blood lymphocytes from non-cancer patients were positive for SV40 genome, and Martini et al. (4) detected SV40 DNA sequences in PBMC from 25% of healthy volunteers and in sperm from 45% of healthy volunteers.

On the other hand, Shah et al. (5) was unable to identify SV40 genome in the urine of homosexual men. Recovery of infectious SV40 from human patients has been reported infrequently (reviewed in reference 6). The frequency of detection of SV40 DNA sequences suggests that most SV40 infections do not have long-term health consequences.

Nevertheless, SV40 infection has been proposed as a possible cause of mesotheliomas (7), ependymomas and other brain tumors (, non-Hodgkin lymphomas (9–11), and bone tumors (12). Consequently, considerable attention has been focused on the possibility of human SV40 infections and the implications for public health (13).

Like other polyoma viruses, SV40 is renotropic and is believed to establish a latent infection in the kidney after primary infection (6). Rhesus monkeys coinfected with simian immunodeficiency virus and SV40 develop acute tubulointerstitial nephritis (14). Butel et al.(15) found SV40 seropositivity in children in association with renal transplantation and amplified SV40 genome from renal transplant biopsies, suggesting for the first time that SV40 might replicate in human kidney (16). The route of transmission SV40 and its possible role in human kidney disease remain to be defined.

Interestingly, expression of SV40 large T antigen in transgenic mouse kidney results in focal segmental glomerulosclerosis (FSGS) (17). FSGS is a renal pathologic syndrome that shares a common histopathologic appearance but likely has diverse etiologies (18). The pathogenesis of FSGS is unclear, although the incidence of FSGS has risen considerably during the past 20 yr, and a new form, collapsing FSGS, emerged about 1980 (19). FSGS affects African Americans to a disproportionate extent. FSGS may be associated with viral infections, including HIV-1 (20) and possibly parvovirus B19 (21,22).

We now report the further evidence that human kidney can harbor SV40 and that patients with kidney disease shed the virus into urine more frequently that do controls. These data suggest that SV40 infections are occurring in the human population and suggest a possible link of SV40 with human kidney disease.

 

[TahoeBlue]

http://cjasn.asnjournals.org/content/2/Supplement_1/S36.full
BK Virus Nephropathy and Kidney Transplantation
Daniel L. Bohl, and Daniel C. Brennan
doi: 10.2215/​CJN.00920207
CJASN July 2007 vol. 2

...

Three polyomaviruses—JCV, BKV, and SV40—cause disease in humans. Humans are the natural host for JCV and BKV. On the basis of serology, BKV is acquired during childhood, and seroprevalence stabilizes or wanes with increasing age (8,9). In contrast, JCV seroprevalence increases with age. The route of the primary infection may be fecal-oral, respiratory, transplacental, or from donor tissue (10–13). Presumably, during a viremic phase, the virus infects target tissues, including the uroepithelium, lymphoid tissue, and brain (13,14), establishing a latent or permissively lytic infection. SV40, a simian virus, was introduced into the human population through contaminated polio and adenovirus vaccines (15). It can be acquired through close contact with nonhuman primates and may spread at a low rate from person to person (10,16,17).

Although SV40 has been identified in kidney transplant biopsies and associated with native kidney diseases (18–21), its importance in kidney transplantation is poorly defined and is not discussed further.

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http://www.researchgate.net/publication/7888439_Human_Polyoma_Virus_in_Kidney_Transplants_SV40_T-Antigen_Demonstration_in_the_Urine
Human Polyoma Virus in Kidney Transplants: SV40 T-Antigen Demonstration in the Urine
University of Helsinki, Helsinki, Uusimaa, Finland
Transplantation Proceedings  (Impact Factor: 0.98). 04/2005; 37(2):945-6. DOI: 10.1016/j.transproceed.2004.12.073
Source: PubMed

ABSTRACT We wanted to develop an immunostaining method of urine cytopreparations to detect polyoma virus infection by using fresh urine samples and staining with the monoclonal SV40 antibody and to compare the findings to the demonstration of decoy cells in the urine or to kidney histology. Routine urine samples from pediatric kidney transplant patients were collected either early after transplantation or later, cytocentrifuged, and immunostained with SV40-T-antibody. The number of SV40-T-antigen-positive epithelial cells was counted in the cytopreparations and compared to the findings in routine urine cytology and transplant histology. Immunostaining of urine cytology with SV40-T-ab demonstrated clearly that the infected epithelial cells and the rate of infection could be estimated by semiquantitative counting. There was strong correlation between the findings in the urine and in the biopsies, but in the urine preparations the number of infected cells was much higher than in the biopsies. The high number of SV40-positive cells in the urine also correlated to the severity of clinical infection and to the state of transplant. Immunostaining of urine cytology with SV40-T-antibody seems to be useful in the diagnosis and follow-up of polyoma virus reactivation disease in transplant patients, especially in children with renal transplants.
...

http://www.ncbi.nlm.nih.gov/pubmed/12490781
Transplantation. 2002 Dec 15;74(11):1497-504.
BK virus and SV40 co-infection in polyomavirus nephropathy.
Li RM1, Mannon RB, Kleiner D, Tsokos M, Bynum M, Kirk AD, Kopp JB.
...

CONCLUSION:

The authors report molecular evidence that co-infection with BKV and SV40 occurs in renal transplant patients with PVN, suggesting that SV40 may contribute to PVN after renal transplant.

[TahoeBlue]

I can't reference this article enough :

It looks like 5 percent of the populations in UK and US have SV40 in their bodies ...
 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC452549/
Clin Microbiol Rev. 2004 Jul; 17(3): 495–508.
Emergent Human Pathogen Simian Virus 40 and Its Role in Cancer
Regis A. Vilchez1,2 and Janet S. Butel2,*
...
Experimental  data strongly suggest that SV40 may be functionally important in the development of some of those human malignancies...

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HUMAN INFECTIONS BY SV40: OVERVIEW OF THE EVIDENCE

Although the prevalence of SV40 infections in humans is not known, studies conducted over the last three decades indicate that SV40 infections are occurring in child and adult populations today. These included individuals who received potentially SV40-contaminated vaccines, as well as in persons born after 1963 who could not have been exposed to those vaccines (5, 11-14, 17, 18, 25, 26, 28, 40, 46, 49, 55, 62, 63, 66, 67, 71-74, 76, 78, 86, 88, 89, 92, 94, 95, 102, 104, 111, 115, 117, 120, 124, 125, 129, 130, 132, 133). In addition, 19% of newborn children and 15% of infants 3 to 6 months old at the time of receiving the oral contaminated polio vaccine were shown to excrete infectious SV40 in their stools for up to 5 weeks after vaccination (75). It is important to point out that the incidence of SV40 infections linked to those vaccines is not known.

SV40 seroprevalence rates in the general populations of the United States and other countries have ranged from 2 to 20% (13, 78, 95).

However, differences in the methodology and low sensitivity of the assays used in some studies make it difficult to ascertain the actual prevalence of SV40 infections. A report by Shah et al. (99) found that 18% of adult kidney transplant patients had specific neutralizing antibody to SV40.

Another study among adult patients showed the presence of SV40 neutralizing antibodies in 16% of human immunodeficiency virus-infected patients and 11% of individuals not infected with human immunodeficiency virus (49).

Among hospitalized children, the overall prevalence of specific SV40 serum neutralizing antibodies was 6% (12); the SV40 seropositivity among children increased with age (P = 0.01) and was significantly associated with kidney transplantation (P < 0.001) (Table ​(Table1).1).

Recently, a study of the prevalence of SV40 infections showed rates of 9% in Hungary and 4% in the Czech Republic (14). Females had a higher rate of SV40 antibodies than males, reaching 16% in Hungary and 8% in the Czech Republic in certain age groups.

SV40 infections were found in similar proportions in both countries among persons not exposed to potentially contaminated polio vaccines and in subjects vaccinated in the era of SV40-free vaccines. Minor et al. (78) recently analyzed over 2,000 sera from the United Kingdom and found an SV40 seroprevalence rate of just under 5%.

Most of the neutralizing titers were low, and there was no apparent relationship between antibody positivity and polio vaccine usage. These data suggest that SV40 is being transmitted in the human population today, probably at a relatively low prevalence rate. However, conclusions about seroprevalence rates should be viewed with caution, as very little is known about the human immune response to SV40 infections.
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[TahoeBlue]

http://www.dailymail.co.uk/health/article-3101086/Deaths-cancer-soar-obesity-smoking-living-longer-Disease-second-biggest-killer-worldwide.html
Deaths from cancer soar due to obesity, smoking and living longer:
Disease is now second biggest killer worldwide after heart disease
Percentage of all deaths due to cancer has risen from 12% to 15% between 1990 and 2013, a landmark report on the global burden of disease found
Is now the second leading cause of death after cardiovascular disease
Experts blamed the rise on an ageing population and lifestyle factors
There were 8.2m deaths from cancer and 14.9m new cases in 2013
By Madlen Davies for MailOnline
Published: 11:29 EST, 28 May 2015  | Updated: 12:20 EST, 28 May 2015
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Comments
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thriveaaa, oxford, United Kingdom, 3 months ago

Mate go and get those tumours tested for sv40 cancer virus.

Sv40 cancer virus was "accidentally" introduced into the polio vaccine in he 50-60s. Back then a award winning scientist predicted these children will go on to develop cancer in their late middle ages.

There has been a growing number of people taking their children's tumours to be tested, and found they have it. One parent has even dedicated an entire website on their 2 year old sons cancer, which had the virus in it. The sv40 cancer virus replicates itself and passes down the bloodline.


Read more: http://www.dailymail.co.uk/health/article-3101086/Deaths-cancer-soar-obesity-smoking-living-longer-Disease-second-biggest-killer-worldwide.html#ixzz3mrjcSBkN
Follow us: @MailOnline on Twitter | DailyMail on Facebook

[TahoeBlue]

One thing that is clear , they never want to refer to SV40 in a paper ... so instead they use the term "Polyomaviruses" as a generality that includes SV40 ... of course a person may get BK because they were infected with sv40 ... so they screen for BK but not for sv40 .. Get it?  ie BKV is the result of SV40

One reason SV40 came up was the development of renal transplants and the failures that occurred ...

example:

http://www.ucsfcme.com/2012/slides/MMC13001/11.%20David%20Wojciechowski.pdf
Screening and Treatment Strategies for BK Virus in Kidney Transplant recipients

http://www.ncbi.nlm.nih.gov/books/NBK6388/
Polyomavirus-associated Nephropathy in Renal Transplantation: Critical Issues of Screening and Management

Polyomavirus-associated nephropathy (PVAN) is an emerging disease in renal transplant patients with variable prevalence of 1-10% and graft loss up to 80%. BK virus (BKV) is the primary etiologic agent, but JC virus (JCV) and possibly simian virus SV40 may account for some cases. Intense immunosuppression is viewed as the most important risk factor.
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The virological aspects of BKV, JCV and SV40 have been described in detail (see Chapters 1, 6, 20). BKV and JCV are specific for the human host and despite a high degree of genetic homology of >70% are independently transmitted from one another
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Thus, polyomavirus genomes resemble (mini-)chromosomes, yet without access to their hosts' germline remain dependent on a minimal set of functions to reach out and colonize to the next generation by infection. In contrast, human exposure to the simian virus SV40 resulted accidentally from contaminated polio- and adenovirus vaccines in the 1960s. Significant spread of SV40 among humans is not supported by serological data, but a role in disease has been put forward by some.15 Possibly, accidental exposure may be ongoing in areas with significant contacts to macaques e.g., in animal parks in rural areas of developing countries.



http://www.researchgate.net/publication/5492646_SV40_Infection_Associated_With_Rituximab_Treatment_After_Kidney_Transplantation_in_Nonhuman_Primates
SV40 Infection Associated With Rituximab Treatment After Kidney Transplantation in Nonhuman Primates
Available from: Akira Kanamoto,  March 27, 2008 

*SV40: simian virus introduced to the population through contaminated polio and
adenovirus vaccines


[ Here this paper shows 10 Percent of the organ donors were infected with SV40: ]

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361282/
Role of simian virus 40 in cancer incidence in solid organ transplant patients
Br J Cancer. 2006 May 22;

Transplant recipients have an increased risk of developing cancer in comparison with the general population. We present here data on cancer development in transplanted subjects who received organs from donors whose DNA was previously examined for the genomic insertion of Simian Virus 40 (SV40). Active follow-up of 387 recipients of solid organs donated by 134 donors, not clinically affected by cancer, was performed through the National Transplant Center (NTC). The average length of follow-up after transplant was 671±219 days (range 0–1085 days). Out of 134 proposed donors, 120 were utilised for organ donation. Of these, 12 (10%) were classified as positive for SV40 genomic insertion. None of the 41 recipients of organs from SV40 positive donors developed a tumour during the follow-up. In all, 11 recipients of organs given by SV40 negative donors developed a tumour (cancer incidence: 0.015 per year). In conclusion, cancer rates observed in our study are comparable to what reported by the literature in transplanted patients. Recipients of solid organs from SV40 positive donors do not have an increased risk of cancer after transplant. The role of SV40 in carcinogenesis in transplanted patients may be minimal.

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In this paper show the association of BK to SV40 :

http://ndt.oxfordjournals.org/content/early/2012/12/18/ndt.gfs537.full.pdf
Nephrol Dial Transplant (2012) 1–10
BK polyoma virus nephropathy in the native kidney
December 18, 2012

Abstract
Background. While BK polyoma virus nephropathy (PVN) is a well-recognized cause of renal allograft dysfunction, PVN of native kidneys is likely under-recognized.
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Pathology showed BK PVN with characteristic intranuclear inclusions staining positive for SV40 T antigen and negative for JC virus (JCV), with positive serum and/or urine PCR for BK virus.

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In the general population, 70–90% of healthy individuals carry antibodies to BKV and have latent non-productive infections in the urogenital tract

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The precise mode of transmission of PV in the general population is unclear. In addition to respiratory infection, feco-oral and transplacental routes of infection may occur. PV has also been isolated from urine, semen, genital organs and skin biopsies

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PVN was confirmed by positive SV40 immunostain in all eight cases

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[worcesteradam]

Injecting viruses past peoples natural defences is apparently not a risk whatsoever, especially those viruses like sv40 which are linked to sarcomas.

But cigarettes, alcohol and obesity are all obvious medical causes of cancer because... statistics.

Right. Ok then.

[TahoeBlue]

searching: "sv40 positive donors"

Here they conclude that they are in fact evidence of SV40 in brain tumors et al ...

http://www.researchgate.net/profile/Katia_Scotlandi/publication/11445201_Different_simian_virus_40_genomic_regions_and_sequences_homologous_with_SV40_large_T_antigen_in_DNA_of_human_brain_and_bone_tumors_and_of_leukocytes_from_blood_donors/links/541af1ae0cf203f155ae66b6.pdf

Different Simian Virus 40 Genomic Regions and Sequences Homologous with SV40 Large T Antigen in
DNA of Human Brain and Bone Tumors and of Leukocytes from Blood Donors

BACKGROUND. Many studies found only a small fragment of the large T-antigen coding sequences in human tumors, raising doubts on authenticity of SV40 sequences detected in these samples.

METHODS. Five different regions of SV40 DNA were investigated in 106 fresh human tumor biopsies (25 brain, 69 bone, 12 Wilms’ tumors), 71 tumor-derived cell cultures (38 from brain and 33 from bone tumors) and normal tissues (5 fresh bone biopsies and 38 buffy coats) by polymerase chain reaction (PCR) techniques and filter hybridization with specific oligoprobes. Expression of SV40 Tag sequences
was analyzed in human tumor specimens by RT-PCR.

RESULTS. SV40 large T-antigen sequences were detected at high prevalence, in human biopsies of primary brain (37–44%) and bone (21–37%) tumors, in cell cultures derived from brain (30–54%) and bone (53–80%) tumors.

SV40 Tag sequences were detected in 29% of buffy coats of blood donors. However, only four brain tumor cell lines showed all the five regions of the SV40 genome investigated.
Expression of SV40 Tag sequences was found in 11 of 27 (41%) human tumor samples.

DNA sequence analysis indicated that the PCR-amplified products belong to the SV40 wild type. Polymerase chain reaction products of Tag middle portion from 20 of 78 (26%) samples showed a 97% homology with telomeric sequences of human chromosomes 10 and 11.

CONCLUSIONS. Authentic SV40 sequences were detected in human samples. The expression of SV40 Tag sequences indicates that SV40 could play a role, as a cofactor, in the onset/progression of specific human cancers. The inability to detect some regions of the virus genome may suggest that those regions are not required for tumor persistence or growth and have been lost or, alternatively, may be the result of assay conditions that were unable to PCR-amplify those regions in the tumors.

Cancer 2002;94:1037–48. © 2002 American Cancer Society.
DOI 10.1002/cncr.10272
KEYWORDS: SV40, tumor, leukocyte, DNA homology.

[TahoeBlue]

again searching: "sv40 positive donors"

http://jvi.asm.org/content/77/2/1595.full
Simian Virus 40 Sequences in Human Lymphoblastoid B-Cell Lines
Accepted 17 October 2002
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Abstract

Human Epstein-Barr virus-immortalized lymphoblastoid B-cell lines tested positive by PCR for simian virus 40 (SV40) DNA (22 of 42 cell lines, 52.3%). Blymphocytes or tissues from which B-cell lines derived were also SV40 positive.
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Lymphoblastoid B-cell lines (n = 4) infected with SV40 remained SV40 positive for 4 to 6 months. SV40-positive B-cell lines were more tumorigenic in SCID mice than were SV40-negative cell lines (4 of 5 [80%] SV40-positive cell lines versus 2 of 4 [50%] SV40-negative cell lines). These results suggest that SV40 may play a role in the early phases of human lymphomagenesis.

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These results confirm and extend previous findings indicating that SV40 is present in PBMCs from oncologic patients and blood donors (1, 6, 12-14, 20; Martini et al., letter) and provide additional evidence indicating that B lymphocytes may constitute a reservoir for SV40 or an SV40-like agent in humans.

Our results also support the hypothesis that SV40 may be transmitted among humans, as has been suggested recently by the detection of SV40-neutralizing antibodies in human immunodeficiency virus-negative and -positive patients (9).

Although we did not observe spontaneous SV40 production from our SV40-positive LCLs, probably because of the low number of SV40-carrying cells, we demonstrate here that LCLs are able to release SV40 virions upon infection with exogenous SV40. These results are consistent with the possibility that B lymphocytes may also be responsible for the spreading of the virus in vivo, at least in the early phases of infection.

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Our observation that SV40 may successfully infect and persist within human B cells, at least for 4 to 6 months, constitutes an important prerequisite for further assessment of whether the virus has a role in the development of B-cell lymphoproliferative disorders.

In this respect, the detection of Tag mRNA expression and the slightly increased tumorigenicity of SV40-positive LCLs are consistent with the possibility that SV40 contributes to human lymphomagenesis.

However, it should be noted that EBV per se is sufficient to immortalize B lymphocytes and sustain their growth when transplanted into SCID mice, thus limiting the possibility of disclosing and adequately evaluating the growth advantage possibly conferred by SV40 both in vitro and in vivo. Our findings, together with the recent demonstration of hepatocyte growth factor/MET autocrine and paracrine loops in SV40-transformed human mesothelial cells (5), should stimulate further studies aimed at elucidating whether SV40 has a contributory role in the development of human B-cell lymphomas.

[TahoeBlue]

I found this interesting ... Deceased Organ donors ARE NOT SCREENED FOR SV40 ...
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http://www.ncbi.nlm.nih.gov/pubmed/23711196
Epub 2013 May 24.

Deceased organ donor screening for HIV, hepatitis B, and hepatitis C viruses: a survey of organ procurement organization practices.

Theodoropoulos N1, Jaramillo A, Ladner DP, Ison MG.

Abstract

Although Organ Procurement and Transplantation Network (OPTN) policy requires that all potential deceased organ donors are screened for human immunodeficiency (HIV), hepatitis B (HBV) and hepatitis C (HCV) viruses by serology, no current policy requires the use of nucleic acid testing (NAT) for organ donor screening.
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http://tpis.upmc.com/tpislibrary/Resident_Handout_2010.pdf
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BK Virus Infection in Transplant Recipients: An Overview and Update
Key words: BK virus, epidemiology, JC virus, kidney, pathobiology, pathogenesis, polyomavirus, renal,
SV40 virus, transplantation
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Historical Aspects
BKV was first isolated in 1970 from a Sudanese kidney transplantation recipient with a ureteric stricture. Epidemiological studies showed that up to 90% of some human populations become exposed to BKV by adulthood.

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Virology
Polyomavirus BK virus (BKV) is a double-stranded DNA virus with a 5-kb genome. It has been classified in the Polyomaviridae family, which includes JC virus (JCV), a well known cause of progressive multifocal leukoencephalopathy, and the simian virus SV40 (1)

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Chronic Alloimmune Injury/Rejection versus Non-Immune Injury

Chronic polyomavirus infection can lead to IF/TA with chronic inflammation—intranuclear viral inclusions, highlighted on immunostaining for the SV40 large T antigen, are diagnostic of infection,
though they may be sparse or even absent in very late fibrotic stages of polyoma virus nephropathy (10). Many recurrent and de novo glomerular or vascular diseases can also lead to glomerulosclerosis and IF/TA, both early and late post-transplant. In addition, de novo diabetic changes are becoming more common in allografts. All of these specific causes of IF/TA can and should be recognized by the
pathologist (Table 1).

[ sv40 Maybe tested for livers ? kidneys? ]


https://www.healthnet.com/static/general/unprotected/pdfs/national/policies/LiverTransplant.pdf
Liver Transplantation Mar 15 1
National Medical Policy
Subject: Liver Transplantation
Policy Number: NMP327
Effective Date*: March 2007
Updated: March 2015

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Currently, lentiviral vectors for research and gene therapy are produced from 293-T cells that are transiently transfected with plasmids encoding the vector and helper functions. However, transiently transfected vectors as well as the presence of SV40 virus large T-antigen (T-Ag) cause serious technical and safety considerations.
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Not Medical Necessary
Health Net, Inc. considers any of the following not medically necessary because there is a paucity of peer-reviewed literature and no current ongoing clinical trials or studies. In addition, many of the current studies involve animals:

 SV40 and lentiviruses



http://www.sv40foundation.org/articles.html

SV40 Cancer Articles

There are over 3,400 scientific articles with SV40 in the title and over 15,000 articles that mention or discuss SV40. This list, therefore, is far from comprehensive, but only provides an example of some articles by experts in the field.

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Government Scientists Compromise SV40 Study

Presently there are over 61 reports from 49 different laboratories that have detected SV40 in human mesothelioma, lymphoma, brain and bone tumors, versus three reports, two from Dr. Shah's laboratory who performed his study under contract from Dr. Strickler at the Viral Epidemiology Branch (VEB) National Cancer Institute (USA) that have failed to detect SV40 in some of these same tumor types.

To address whether the negative reports were caused by lack of sensitivity of the technique used in Shah's laboratory, or whether the positive reports were caused by contamination within the greater number of laboratories reporting SV40 detection, two multi-center studies were conducted. Dr. Shah's laboratory technique used in 1996 was apparently not sufficiently sensitive to detect SV40 in human tumors. When this became apparent, during unilateral pre-trial testing of positive controls by Dr. Shah, the study coordinator of the VEB, Dr. Strickler, apparently compromised the blinded nature of the study and allowed Dr. Shah to modify and improve his technique. When one of the participating laboratories questioned irregularities in the data from Dr. Shah's laboratory and directly questioned Dr. Strickler, the study organizer, about the potential irregularity, Dr. Strickler and Dr. Shah offered letters stating that such irregularities had not occurred and re-confirmed that they had not deviated from the standard protocol. The facts indicating that Dr. Shah's laboratory technique was not sufficiently sensitive to detect SV40 were not made available to the other laboratories participating in the study and were not published. Instead, according to Dr. Shah's testimony, Dr. Strickler, the VEB multi-center study coordinator, compromised the masked positive controls and knowingly permitted Dr. Shah to re-test and adjust his technique during pre-trial testing. The actual negative pre-trial test results were never published alongside the published trial results indicating Dr. Shah's laboratory had the most sensitive technique to detect SV40 among the nine participating laboratories.

[TahoeBlue]

Interesting population distribution of BK polyomavirus (BKV)  Virus:


http://www.ncbi.nlm.nih.gov/pubmed/19088283
J Gen Virol. 2009 Jan ;90(Pt 1):144-52. doi: 10.1099/vir.0.83611-0.

Distribution patterns of BK polyomavirus (BKV) subtypes and subgroups in American, European and Asian populations suggest co-migration of BKV and the human race.
Zhong S1, Randhawa PS, Ikegaya H, Chen Q, Zheng HY, Suzuki M, Takeuchi T, Shibuya A, Kitamura T, Yogo Y.

Abstract

BK polyomavirus (BKV) is ubiquitous in the human population, infecting children asymptomatically and then persisting in the kidney.

Based on serological and genotyping methods, BKV isolates worldwide are classified into four subtypes (I-IV), with subtype I prevalent throughout the world, subtype IV prevalent in Asia and part of Europe, and subtypes II and III rare throughout the world.

Phylogenetic analyses of complete genome sequences have identified several geographically distinct subgroups of subtypes I and IV.

To explain how the geographical distribution patterns of BKV subtypes and subgroups were formed, this study hypothesized that BKV co-migrated with human populations (the co-migration hypothesis), and examined this hypothesis by comparing the BKV subtype and subgroup profiles among two American populations in North-east USA and southern California, two European populations in Finland and Ireland/England, and two Asian populations in Japan and China (both American populations were composed mainly of European Americans).

The frequency of subtype I was always the highest throughout the populations, but that of subtype IV was variable among populations. A subgroup of subtype I (I/b-2) was detected primarily in all of the European and American populations, whereas subgroup I/c was predominant in the Asian populations (the observed difference was statistically significant).

Additionally, all of the five fully sequenced subtype IV isolates from the American and European populations belonged to subgroup IV/c-2, whereas all subtype IV isolates from the Asian populations belonged to the other subgroups. Collectively, the current findings provide support for the co-migration hypothesis.