NOTE: I know next to nothing about microbiology or vaccines. However people are being paid many millions of dollars to advance in directions proven to be harmful to humans and unnecessary to human health. In fact in some of these cases, reaction to adjuvant etc. is worse than the disease supposedly targeted by an adjuvated vaccine.
As most of you know, adjuvants used in vaccines in America's past have caused GBS or Guillian-Barre Syndrome.
Landry-Guillain-Barre syndrome; Acute idiopathic polyneuritis; Infectious polyneuritis; Acute inflammatory polyneuropathy; Acute inflammatory demyelinating polyneuropathy
Last reviewed: June 15, 2010.
U.S. National Library of Medicine
National Institutes of Health
National Center for Biotechnology Information
U.S. National Library of Medicine
National Institutes of Health
Guillain-Barre syndrome is a serious disorder that occurs when the body's defense (immune) system mistakenly attacks part of the nervous system. This leads to nerve inflammation that causes muscle weakness.
Causes, incidence, and risk factors
Guillain-Barre syndrome is an autoimmune disorder (the body's immune system attacks itself). Exactly what triggers Guillain-Barre syndrome is unknown. The syndrome may occur at any age, but is most common in people of both sexes between ages 30 and 50.
It often follows a minor infection, such as a lung infection or gastrointestinal infection. Most of the time, signs of the original infection have disappeared before the symptoms of Guillain-Barre begin.
The swine flu vaccination in 1976 may have caused rare cases of Guillain-Barre syndrome. However, the swine flu and the regular flu vaccines used today have not resulted in more cases of the illness.
Guillain-Barre syndrome damages parts of nerves. This nerve damage causes tingling, muscle weakness, and paralysis. Guillain-Barre syndrome most often affects the nerve's covering (myelin sheath). Such damage is called demyelination, and it causes nerve signals to move more slowly. Damage to other parts of the nerve can cause the nerve to stop working altogether.
Guillain-Barre syndrome may occur along with viral infections such as:
It may also occur with other medical conditions such as systemic lupus erythematosus or Hodgkin's disease.
Some people may get Guillain-Barre syndrome after a bacterial infection. A similar syndrome may occur after surgery, or when someone is critically ill (neuropathy of critical illness).
The controversial Anthrax vaccine was adjuvated with a substance called squalene. There were cases of GBS reported or the CDC would not have said this:
Some people should not get anthrax vaccine.
* Anyone who has had a serious allergic reaction to a previous dose of anthrax vaccine should not get another dose.
* Anyone who has a severe allergy to any vaccine component should not get a dose. Tell your provider if you have any severe allergies, including latex.
* If you have ever had Guillain Barré syndrome (GBS), your provider might recommend not getting anthrax vaccine.
* If you have a moderate or severe illness your provider might ask you to wait until you recover to get the vaccine. People with mild illness can usually be vaccinated.
* Vaccination may be recommended for pregnant women who have been exposed to anthrax and are at risk of developing inhalation disease. Nursing mothers may safely be given anthrax vaccine.
This information was taken directly from the VIS Adobe Acrobat print-friendly PDF file [PDF - 72KB]
(This information taken from Anthrax VIS dated 3/10/10. If the actual VIS is more recent than this date, the information on this page needs to be updated.)
Now that we have talked about adjuvants the media has already discussed, it's time to talk about the new adjuvant being used in the soon to be mandatory malaria vaccine:
CD1d/NKT-binding glycolipids as an adjuvant for T cell-based HIV and malaria vaccines
The eradication of global pathogens responsible for endemic and pandemic diseases hinges upon the development of effective vaccines. This is certainly the case for HIV and malaria. However, our inability to elicit “strong and long-lasting” protective T cell responses, particularly CD8+ T cell responses, has been a major obstacle to successful vaccine development. Accordingly, adjuvant technologies will likely be critical not only to overcome pre-existing immunity to viral vaccine vectors but also to further enhance vaccine immunogenicity. Our previous studies have demonstrated that a CD1d molecule-binding, natural killer T (NKT) cell ligand, alpha-galactosylceramide (alpha-GalCer), can enhance protective CD8+ T cell responses elicited by HIV and malaria vaccines, including a DNA vaccine encoding HIV antigens and a recombinant adenovirus expressing a malarial antigen. In collaboration with two eminent chemistry groups directed by Dr. Chi-Huey Wong and Dr. Richard Franck, we have successfully identified several alpha-GalCer analogues that act as an NKT cell ligand. These include a synthetic C-glycoside analogue, alpha-C-GalCer (JEM in 2003 and PNAS in 2005), a sulfatide analogue, 3-O-sulfo-GalCer (PNAS in 2005), two bacterial glycosphingolipids, GSL-1A and GSL-1B, derived from Sphingomonas (Nature in 2005), and a diacylglycerol from Borrelia burgdorferi (Nature Immunology in 2006). Our most recent results indicate that introduction of a phenyl group at the end of eight fatty acid carbon chain yielded activities superior to alpha-GalCer (JACS in 2006). Thus, concrete clues on the structure-activity-relationship (SAR) are emerging from our preliminary studies on an initial library screening of glycolipids. We are continuing to screen a focused library of several hundreds alpha-GalCer analogues that we are generating, and selecting a smaller panel of candidate glycolipids based on their in vitro cytokine production profiles upon cultivation with murine and human NKT cells. We are also determining the in vivo cytokine production profiles elicited by the selected glycolipids upon administering them into mice. These in vitro and in vivo screening process will lead us to choose about a handful of promising candidate glycolipids that would display strong Th1-biased, Th2-biased, or bipolar activities. These glycolipids having a distinct biological activity will present us an opportunity to determine the means by which glycolipids elicit Th1 versus Th2 cytokine secretion, in collaboration with Dr. Mitchell Kronenberg at La Jolla Institute of Allergy & Immunology. Ultimately, we plan to determine the magnitude of adjuvant effect that each of these newly identified glycolipids contributes to the immunogenicity of HIV and malaria vaccines in a mouse model.
Now please read the following regarding anti-glycolipid action in GBS victims:http://www.gbs-cidp.org/newsletters/printer%20versions/anti-glycolipid%20antibodies%20in%20GBS.htm
Since the mid-1980s, there has been remarkable progress in our understanding of the clinical pathophysiology of autoimmune neuropathies that shows no sign of slowing down, particularly the continued identification and analysis of antibodies to gangliosides and related glycolipids in the serum of patients. Antiglycolipid antibodies react with epitopes on the carbohydrate region of glycolipid molecules and can be routinely measured by standard immunoassays. From a clinical diagnostic perspective, they are very useful. For example, in multifocal motor neuropathy, IgM anti-GM1 antibodies are detectable in around 50% of cases. This condition clinically resembles lower motor neuron disease. IgM anti-GD1b antibodies are found in IgM paraproteinaemic neuropathy characterized by profound sensory ataxia. In the anti-myelin associated glycoprotein (anti-MAG) IgM paraproteinaemic neuropathy, antibodies also react with the acidic glycolipids, sulphated glucuronyl paragloboside and its higher lactosaminyl homologue (SGPG and SGLG). Thus a variety of chronic syndromes can be defined by their anti-glycolipid antibody profile and those interested in supporting GBS should not forget the importance of this group of closely related chronic neuropathy syndromes.
In Guillain-Barrp syndrome, anti-GM1, GM1b, GD1a and GalNAc-GD1a antibodies are found in patients with the GBS variant termed acute motor axonal neuropathy (AMAN). These antibodies tend to be IgG class, arise transiently following preceding infections, especially Campylobacter jejuni, and disappear concomitant with clinical recovery. Molecular mimicry (the sharing of antigenic determinants between microbial and host carbohydrate structures) is believed to be the principle mechanism by which they arise. In the acute inflammatory demyelinating polyneuropathy (AIDP) pattern of GBS that is predominant in the USA and in Europe, anti-glycolipid antibodies are less commonly found, although are certainly present in a proportion of cases. GBS occurring in association with Cytomegalovirus infection has been linked with anti-GM2 antibodies. Affected patients have prominent sensory symptoms and cranial nerve involvement. Mycoplasma pneumonia infection preceding GBS is occasionally found in association with anti-GalC antibodies. The significance of finding antibodies to CalC lies in the experimental demonstration that they are capable of inducing morphological and electrophysiological evidence of demyelination. Anti-LM1 and SGPG antibodies have also been reported in AIDP. Understanding this area in more detail remains one of the most pressing areas for research. Are these types of antibodies more frequently present, but hiding for our view, or are they absent in many cases? If the former is the case, we should be looking harder; if the latter is the case, we should be looking elsewhere. In practice both these avenues are being pursued in laboratories around the world.
Miller Fisher syndrome (MFS), or Fisher’s syndrome is the regional variant of GBS that has been of great interest to me since the discovery of anti-GQ1b antibodies. MFS accounts for 5-10% of cases and was first described in 1956 as the clinical triad of ophthalmoplegia, ataxia and areflexia. Since then MFS has evolved as a nosological entity to take into account closely related variants, principally characterized by acute cranial neuropathy with ataxia. Bickerstaff described a now eponymous syndrome in which MFS occurs in conjunction with brain stem involvement, comprising pyramidal tract signs and impaired consciousness. Anti-Go1b ganglioside antibodies were first identified in MFS in a landmark study published in 1992 and this has since been substantiated in many other reports. Anti-GQ1b antibodies are a very sensitive and specific marker ofr MFS and related syndromes characterized by ophthalmoplegia. Anti-GQ1b antibodies are present in over 90% of cases during the acute phase but may disappear rapidly, often being absent during convalescence.
* Performing your original search, glycolipids gbs, in PubMed will retrieve 357 records.
J Neurol Sci. 1992 Jan;107(1):111-21.
Antibodies to acidic glycolipids in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy.
Ilyas AA, Mithen FA, Dalakas MC, Chen ZW, Cook SD.
Department of Neurosciences, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark 07103.
Using an enzyme-linked immunosorbent assay and a thin-layer chromatography-immunostaining procedure, we detected serum antibodies against acidic glycolipids in 36 of 53 patients with Guillain-Barré syndrome (GBS) and 8 of 16 patients with chronic inflammatory demyelinating polyneuropathy (CIDP). Although we also found anti-acidic glycolipid antibodies in 4 of 13 patients with other neurological diseases; 2 of 10 patients with multiple sclerosis; 8 of 33 patients with inflammatory, infectious, allergic or autoimmune disorders and 3 of 32 healthy subjects, the levels of antibodies in these controls were much lower than in GBS patients. There were several patterns of reactivity of GBS sera including antibodies to LM1 and HexLM1, GM1 or GD1b or both, various other gangliosides, sulfated glycolipids, and as yet unidentified glycolipids. Sera from 30% of GBS patients had antibodies against two or more antigenically distinct acidic glycolipid antigens. Levels of anti-acidic glycolipid antibodies correlated with clinical symptoms in 9 of 11 GBS patients. While the increased incidence of antibodies to acidic glycolipids in patients with GBS (P less than 0.001) and CIDP (P less than 0.025) compared to controls could be an epiphenomenon, anti-acidic glycolipid antibodies may play a role in nerve injury in some GBS and CIDP patients.
PMID: 1578228 [PubMed - indexed for MEDLINE]
Basic neurochemistry: molecular, cellular, and medical aspects, Volume 1
By George J. Siegel, R. Wayne Albers
Enhancing Nerve Repair in GBS and CIDP
Kazim A. Sheikh, M.D., Department of Neurology, University of Texas Health Sciences Centre, Houston, TX
Guillain-Barre syndrome (GBS) and Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are considered to be organ specific immune disorders resulting from synergistic actions of cellular and humoral autoimmune responses directed against peripheral nerve antigens. Current therapies for the treatment of these conditions are directed at modulating abnormal autoimmune responses. The recovery process in both disorders requires curtailment of autoimmune injury and nerve repair. The natural nerve repair process is often very slow and incomplete and patients are left with residual deficits. The patients with residual damage almost always have failure of axon regeneration and reconnection with targets such as muscle or skin. We have found that immune effectors including some autoantibodies interfere with the process of axon regeneration. Our latest studies indicate that nerve damage induces expression of new injury-related proteins that are not expressed in normal nerves. Some of these proteins serve as receptors to capture immune molecules such as antibodies to form molecular complexes that interact with injured axons attempting to regenerate and prevent the process of nerve repair. The deleterious effects of the immune molecules on nerve repair are enhanced due to the formation of these complexes, which allow the immune molecules to stay in the nerve compartment for longer and also allow them interact with their target molecules more effectively.
There is lot of interest in developing new therapies that can enhance nerve repair and taking them to the clinical arena. Our group is also examining at new approaches that can enhance nerve repair to treat neuropathic conditions such as GBS and CIDP. In our initial studies we have found that recombinant human erythropoietin (EPO), an FDAapproved drug, significantly enhances nerve repair in preclinical models of autoimmune neuropathy. We are now in the process of generating genetically engineered modified forms of EPO that would allow the modified-EPO to interact with the same new proteins that are expressed in injured nerves and capture immune molecules such as antibodies to form complexes (see above). We believe that the modified-EPO will be captured by injury-related proteins expressed in the nerve to form complexes and this will allow modified EPO to stay longer in the nerve compartment and interact more avidly with its receptors to enhance axon regeneration/nerve repair more effectively than na?ve unmodified EPO. These GBS and CIDP Foundation sponsored studies are currently being carried out in our laboratory.
Acknowledgements: Sponsors GBS/CIDP Foundation International
C-glycolipid antibody gbs
method of binding
method of adjuvating
link between adjuvant and GBS
There is a link between mycoplasmas, the way the body reacts to mycoplasmas, and the similarities between human proteins and the marker proteins of these invading organisms; once infected with a mycoplasma there is a chance that your body will attack its own nerve tissue, hence the myelinopathy; also if injected with glycolipid in conjunction with other immune irritants, GBS symptoms may also present.
There is something weird about all this, the common thread between GBS, GWS, H1N1, vaccines, mycoplasmas, etc.
There are common factors between AIDS, Herpes, GBS, demyelinating diseases...
someone with science background should read some of this.
The mycoplasma and anything with its properties, it has no business being in our vaccines in the amounts sometimes found; it was suspected as a contaminant in mid 1980s vaccines and may even have caused or played a part in AIDS.
Mycoplasmas have no cell wall and can simply hitch a ride in your Tcells and propagate wherever other infections are present.
It's scary and sick!
Not to mention Venter and his shitheads have the whole organism mapped, undoubtedly understand what it does and how, and can mail DNA on demand to eco and bio terrorists around the globe. Mad scientist selling life to the highest and most evil bidders. Giving undreamed of power to the already obscenely powerful. This is undoubtedly the most significant advance that I know of in our time. Yay Bill Gates and everyone else who funded this, maybe you should have watched the purse strings closer, or was this what you wanted all along?
Forced sacrifices rather than willing ones, once we got sick of Planned Molech Worship and illegal wars?