Science fiction or fact?

The question. Did the conditions exist for the current epidemic of neuroimmune diseases to be the result of endogenous retroviruses present in animal tissues and used in the production of vaccines?

Epidemic neuromyasthenia; clinical syndrome?, by Henderson and Shelokov, published in the New Enland Journal of Medicine in 1959, describes what were probably the first cases of ME/CFS. This extraordinary paper lists 23 outbreaks of illness internationally, similar to the Lyndonville and Lake Tahoe outbreaks, between the years of 1934 and 1958.

Preceding the report of the outbreak in Iceland [of 1090 people] were 2 epidemics in the United States and 1 in England, all of which in retrospect, bear it a striking resemblance. Gilliam documents in detail an outbreak in 1934 of 198 cases among personnel at the Los Angeles County General Hospital during which 10 per cent of the 1531 physicians and nurses were afflicted. Occurring concomitantly in Los Angeles and in other areas of California were many cases that were considered typical of paralytic poliomyelitis and a great many others that were not. In addition to a number of hitherto unknown clinical manifestations particularly among adults, epidemiologic appraisal of reported cases revealed an unusually high attack rate, a low paralytic and case fatality rate and a relative age selection for adults, particularly females. Gilliam believed that the symptomatology among the hospital personnel was not characteristic and that the very high attack rate among the hosptial personnel was without parallel in the history of poliomyelitis. He concluded, however, that since classic poliomyelitis prevailed among a large number of the pateints with communcable disease in the hospital, the simpler explanation of the facts was that the atypical disease seen among the hospital staff was the same.

Edward Jenner, as an apprentice to a surgeon, observed that milkmaids who contracted cowpox were afterwards immune to smallpox. He first used cowpox material to produce cross-immmunity in a child in 1796 and, shortly after, reported a series of 23 cases, which included his son. The idea that a weak form of a disease can cause immunity was not new. As early as 1000 BC, it was known that an inoculation, or “variolation”, with material from smallpox lesions (Variola) produced a lighter form of the disease, though still with significant morbidity and mortality. Powdered material from smallpox scabs was blown up the noses of people in China in the 1500’s. It was observed in the early 1700’s that variolation had no effect on people who had had cowpox (Vaccinia).

Louis Pasteur, while working on chicken cholera, discovered that a faulty culture that didn’t kill as expected produced immunity in chickens. He used this concept to develop a post-exposure rabies vaccine. He grew the virus in rabbits, dessicated spinal cord to weaken the virus, and injected the dried product into the first human, an exposed child, in 1895. His treatment was quite successful as documented in this paper: Rabies And The Pasteur Treatment. Lackenbach. 1912. Pasteur’s work with anthrax and chicken cholera was different from Jenner’s in that the vaccine was artificially produced rather than using a naturally weak form of the disease. Pasteur coined the named vaccine from Jenner’s work with cowpox.

A couple of historically interesting papers with respect to the early use of animals to grow viruses for vaccinating humans:

Max Theiler, and his colleagues at Harvard, proved that Yellow Fever was not caused by a bacterium, but a filterable virus. He also proved that the virus could be transferred to monkeys and mice. In 1930, Theiler started working on a Yellow fever vaccine at the Rockefeller Institute, where much of the early vaccine work was done. He attenuated virus in mouse brain and chick embryo cell. Early vaccines were sometimes tested on volunteer doctors. Informative reference: The Yellow Fever Vaccine: A History. Frierson

From Theiler’s Nobel lecture in 1951:

The study of yellow fever may be divided into two periods. The first one occurred at the turn of the century when Walter Reed and his co-workers showed by the use of human volunteers that the causative agent of this disease was a filterable virus and that it was transmitted by the bite of the common urban mosquito, subsequently named Aedes aegypti. The second period began in 1928, when Stokes, Bauer, and Hudson found that the common Indian rhesus monkey was susceptible to yellow fever, thus making available an animal that could be used in the laboratory. The first strain of yellow fever established by these workers is known as the Asibi strain, named after the patient from whom it was isolated. It has been used extensively in yellow fever work and, as will be shown later, was the parent strain from which the 17D vaccine was eventually produced.

It was shortly after monkeys were found susceptible that, in searching for a less expensive and more readily available experimental animal, I found that the common white mouse was susceptible to the virus if inoculated by the intracerebral route. This method of inoculation was chosen as it was generally conceded that the common laboratory animals could not become infected if inoculated by the usual routes. The strain of virus with which this work was done was isolated by Mathis, Sellards, and Laigret in 1928 in Dakar, French West Africa, is known as the French strain, and, like the Asibi, is highly virulent for rhesus monkeys. The disease in mice was an encephalomyelitis with no involvement of the visceral organs, in contrast to that induced in man and monkey, in which the liver, kidney, and heart are involved. By serial passage in mice, the pathogenic action of the virus was altered in two respects. Firstly, the incubation period became progressively shortened until, after many passages, it became constant, or, to use the term introduced by Pasteur in his work on rabies, it became fixed. Now the incubation period in mice is used as a measure of the degree of neurotropism for these animals. Secondly, with the increase of virulence for the nervous system of mice, there was also evidence of a progressive loss of virulence for rhesus monkeys when inoculated parenterally. This loss of virulence for monkeys first suggested the possibility of the use of an attenuated active virus for the immunization of man. The finding that by mouse brain passage the virulence of yellow fever virus could be altered led me to undertake extensive studies on the variations induced in the virus by different laboratory procedures, which became my main scientific activity for several years. The results of only those experiments which are pertinent to the development of vaccines will be discussed here.

The finding of the susceptibility of mice and its attenuation for monkeys was rapidly confirmed by others. It was shown that many, if not all, strains of yellow fever are pathogenic for mice, and this animal came into widespread use in all yellow fever work. The pathogenicity of unmodified strains for mice varied greatly – ranging from the highly neurotropic Asibi virus to the relatively avirulent French strain. Both of these, as noted before, are highly pathogenic for rhesus monkeys and almost invariably produce a fatal disease when inoculated parenterally. With most strains it was shown that the mouse could be used for the quantitative estimation of virus. This proved of great value, for as strains of virus avirulent for monkeys were developed, the mouse was the only animal by which the presence and amount could be readily determined.

In the development of vaccines for human beings, using my mouse-adapted virus, two paths were followed. In the first, used chiefly by French workers, virus alone was inoculated; and in the second, used by American and English workers, virus and human immune serum were inoculated simultaneously. The first immunizations of humans using mouse-adapted neurotropic virus alone were reported by Sellard and Laigret (1932)…   Full lecture

The first attempts to vaccinate for polio were actually in the 1930’s. Live and killed virus was used, passaged in monkey brain and spinal cord. The vaccines were tested on children and it was a fiasco; some of the test subjects developed the disease. For historical interest:

In the late 1940’s Hillary Koprowski worked with rodent and mouse adapted viruses, including rabies, Colorado tick fever, various viral encephalitides, West Nile Virus and others, before turning his attention to polio. He made the earliest live polio vaccine using Swiss albino mouse brain cells. The first dose was administered to a child in 1950. He also used monkey kidney cells which were implicated in passing SV40 to humans. Albert Sabin’s live polio vaccine was produced from attenutated virus obtained from Koprowski. Here are the earliest papers:

So it was probably all a big accident, which occurred for the best of reasons, to remove the scourge of horrible viral diseases from the human race. The ethical problem started later, when there was enough information and technology at hand to understand what was happening and nobody studied it. Instead they decided that the patients were all crazy. Easier to marginalize them. The really sad part is that, certainly by the early ’90s, when De Freitas did her work at Wistar, there was enough information to question whether it was safe to inject endogenous animal retroviruses into humans, even though it was known that they could recombine and infect the cells of other species in tissue culture, including human. They knew the viruses were there, they knew there was risk, but chose to march ahead blindly anyway. Amazing arrogance.

And this paper whose senior author seems to ignore his own work:

J Virol. 2003 Jun;77(12):6709-19.
Mechanisms of avian retroviral host range extension.
Rainey GJ, Natonson A, Maxfield LF, Coffin JM.
Department of Biochemistry, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.

Alpharetroviruses provide a useful system for the study of the molecular mechanisms of host range and receptor interaction. These viruses can be divided into subgroups based on diverse receptor usage due to variability within the two host range determining regions, hr1 and hr2, in their envelope glycoprotein SU (gp85). In previous work, our laboratory described  selection from a subgroup B avian sarcoma-leukosis virus of an extended-host-range variant (LT/SI) with two adjacent amino acid substitutions in hr1. This virus retains its ability to use the subgroup BD receptor but can also infect QT6/BD cells, which bear a related subgroup E receptor (R. A. Taplitz and J. M. Coffin, J. Virol 71:7814-7819, 1997). Here, we report further analysis of this unusual variant. First, one (L154S) of the two substitutions is sufficient for host range extension, while the other (T155I) does not alter host range. Second, these mutations extend host range to non-avian cell types, including human, dog, cat, mouse, rat, and hamster. Third, interference experiments imply that the mutants interact efficiently with the subgroup BD receptor and possibly the related subgroup E receptor, but they have another means of entry that is not dependent on these interactions. Fourth, binding studies indicate that the mutant SU proteins retain the ability to interact as monomers with subgroup BD and BDE receptors but only bind the subgroup E receptor in the context of an Env trimer. Further, the mutant SU proteins bind well to chicken cells but do not bind any better than wild-type subgroup B to QT6 or human cells, even though the corresponding viruses are capable of infecting these cells. Full paper

This paper exists only in print and there is no abstract, but it must be interesting:

Nat Med. 1995 Nov;1(11):1100.
The dangers of xenotransplantation.

There are lots of papers about the dangers of xenotransplantation:

More evidence that avian leukosis viruses can infect human cells under certain circumstances:

And the idea that it only happened once, in a particular cell line? It seems that the chances are not so vanishingly small after all. From an easy to understand review of retroviruses: C-type: As B-type, but with a central core and barely visible spikes – e.g. most mammalian and avian retroviruses (MLV, ALV, HTLV, HIV). All old work:

Cover-up or stupidity? I’m just a dumb ER doc and I’ve gotten this far with PubMed and a few scientist friends (who if asked will deny knowing me:). Though any detail of what I’ve written could be mistaken, and there is conflicting evidence, overall, it certainly seems to fit. People have written that they are concerned that I’m too invested in XMRV. This is not all about XMRV. If they prove tomorrow beyond a shadow of a doubt that XMRV is a lab contaminant and not present in humans, it doesn’t change a thing in terms of what needs to happen next. At the very least XMRV has brought attention to an international disgrace. If XMRV is buried under a mountain of negative studies, or if XMRV is truly not a human pathogen, millions of people still need treatment for neuroimmune illnesses that are consistent with simple retroviral infection.

Certain scientists have been particularly vocal against the use of antiretrovirals for XMRV. Scientists trying to tell doctors what to do. Why do they think that doctors or patients should care about their medical opinions? They need to do their work and stop trying to practice medicine. The real question is why do they care if patients try antiretrovirals for a retrovirus? Why wouldn’t they want to know if the drugs work?

The current epidemic of neuroimmune illnesses may be due to the introduction of simple retroviruses into the human population through the use of vaccines. This hypothesis needs to be studied. I am not some crazy conspiracy theorist. The pathogenesis of the illnesses needs to be further elucidated and specific treatment found. Now. Not after one specific etiologic agent has been deemed the real deal and there’s a foolproof test available at Quest. There may be many specific agents. It’s so unfortunate that it didn’t turn out to be one retrovirus with a serology test that picks up all cases. That would have been so easy compared to what we are facing – infections with one, or more than one, of a panoply of simple retroviruses, that remain latent for long periods of time, are activated by inflammation and steroid hormones, creating a vicious cycle of inflammation and viral replication. It could be that replication incompetent viruses are part of the picture as well. Co-pathogens, like Lyme, fuel inflammation and there may be helper viruses involved in various ways. And, most unfortunately, there is even a possibility that the new simple human retroviruses are or will be endogenized in subsequent generations. What a mess!

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60 thoughts on “Science fiction or fact?

  1. >Great article, thank you.

    To further expand on Dr Deckoff-Jones's concerns it should be noted that the CDC is going to now study the link between Autism and Vaccines. What a strange co-incidence this has happened post XMRV finding in CFS, Autism, Cancers and other neuroimmune disorders.

    Link Below:

  2. >There is plenty of documentation indicating scientific and government agencies have long been aware of the risks associated with the development and use of vaccines and biologics.

    A 1998 document entitled " Guidance for Industry Q5A Viral Safety Evaluation of Biotechnology Products Derived From Cell Lines of Human or Animal Origin" is just one example.

    The following US government agencies are listed under the Heading:

    U.S. Department of Health and Human Services
    Food and Drug Administration
    Center for Drug Evaluation and Research (CDER)
    Center for Biologics Evaluation and Research (CBER)

    Another document "Briefing Document — Testing for Replication Competent Retrovirus (RCR)/Lentivirus (RCL) in Retroviral and Lentiviral Vector Based Gene Therapy Products — Revisiting Current FDA Recommendations" provides this information:

    Retroviral vectors are engineered to be replication defective; however replication competent retroviruses (RCR) may be generated during manufacturing through homologous or non-homologous recombination between the transfer vector, packaging components and endogenous retroviral elements in producer cells (Chong et al. 1998; Garrett et al. 2000). RCR were in fact detected from early generation vector production systems (Miller 1990).

    Many gammaretroviruses are known to cause tumors in animals (Rosenberg and Jolicoeur 1997). After the reported observation that three of ten Rhesus monkeys developed lymphomas after transplantation with cells transduced with a gammaretroviral vector lot that was inadvertently contaminated with RCR (Donahue et al. 1992), FDA began requesting manufacturers and investigators to test the retroviral vector products at multiple stages in manufacturing to ensure absence of contaminating RCR and to monitor the treated patients for evidence of RCR.

    Given the dates, the explosion of biotechnology, and the use of biologics, it makes me wonder if ANY patients and scientists have been tested for exposure to RCR's. Where is the accountability?

    According to the "Guidance for Industry" document referenced above, the "FDA recommends that the most sensitive available methods for RCR or RCL testing be utilized. The current method of choice for RCR/RCL testing is the cell culture based method in which test articles are co-cultured with a highly permissive cell line for amplification followed by endpoint detection of RCR/RCL specific components."

    I have yet to find an updated version of this 1998 document. Regardless, reliable testing needs to occur as soon as possible.

    This leads me to wonder if Quest has licensed technology for detecting XMRV or other threats?

    I can't wait to hear the answer!

    ~ JT

  3. >Excellent, Jamie.

    I wish you'd take this and the previous few posts and weave them together into a piece to submit to Medical Hypotheses.

    "The current epidemic of neuroimmune illnesses may be due to the introduction of simple retroviruses into the human population through the use of vaccines. This hypothesis needs to be studied."

    This is true. I would add that massive chemical onslaught, poor denatured food, heavy metal poisoning, and tickborne illness probably all contribute heavily.

  4. >Mess indeed.

    Now these same scientist, if they wish to remain calling themselves that, should do the job they signed up for and apply the scientific method to investigating this. No more slap dash, let's try a new assay, type paper. Time is being wasted and we don't know if we are actually consigning our race to oblivion.


  5. >What scares me the most is knowing it would take many years to be able to treat the panoply of viruses that are affecting people today, it that is true.

  6. >I see no contradiction in XMRV as a fundamental contributor to CFS.

    The question for me is, why would "CFS" emerge as a discrete phenomenon in a pristine mountain resort high up in the Sierra Nevada Mountains?

    If an accumulation of toxins, stress and stressors from modern life could cause such a thing, the centers of civilization and high concentrations of pollution should have been afflicted first.

    Athletic people living the mountain lifestyle with access to the best air and food available should have been the very last.

    Theories must fit the facts.

  7. >Erik,
    The environmental factor probably caused inflammation that activated the virus, or viruses, in susceptible people.

  8. >>It's so unfortunate that it didn't turn out to be one retrovirus with a serology test that picks up all cases. That would have been so easy compared to what we are facing – infections with one, or more than one, of a panoply of simple retroviruses, that remain latent for long periods of time, are activated by inflammation and steroid hormones, creating a vicious cycle of inflammation and viral replication. It could be that replication incompetent viruses are part of the picture as well. Co-pathogens, like Lyme, fuel inflammation and there may be helper viruses involved in various ways. And, most unfortunately, there is even a possibility that the new simple human retroviruses are or will be endogenized in subsequent generations. What a mess!

    As is the case with Lyme — mercury, certain biotoxins such as toxic mold, and herpes viruses also fuel inflammation.

    These are things that are cited again and again as issues for us, and generally dismissed as downstream. But it's seeming to me more like everything just melds together into one gruesome mess.

    The more that we look at how all these things fit together, the more likely we will be to figure out a way to dig ourselves out.

    I think that this is a really impressive hypothesis and that somebody had damned well better study it. Thank you for your work on it so far.

  9. >"The current epidemic of neuroimmune illnesses may be due to the introduction of simple retroviruses into the human population through the use of vaccines. This hypothesis needs to be studied."

    This is true. I really hope it is studied. We really need some answers.

    Patricia Carter

  10. >Jamie,
    Dr Erich Ryll made the astute observation that the virus was "already in residence" back in 1975 for his Mercy Hospital Infectious Venulitis cohort, whose descriptions were uncannily identical to the Tahoe outbreak.

    (It's amazing what those old-time physicians were capable of deducing long before any testing methods were invented)

    Wouldn't the simultaneous emergence of a dormant or latent virus in so many people in such a short time throw a greater emphasis on whatever reactivated it?

  11. >"This paper exists only in print and there is no abstract, but it must be interesting:
    Nat Med. 1995 Nov;1(11):1100.
    The dangers of xenotransplantation.
    Stoye JP, Coffin JM."

    It seems that this was a letter to the editor of Nature Medicine.

    It starts:
    To the editor — In the September issue of Nature Medicine, Fritz Bach and colleagues contributed to the recent spate of enthusiasm for xenotransplants as a source of organs1. Throughout this episode, there has, however, been little discussion of the dangers posed by the possible activation of endogenous retroviruses2.

    Stoye cited this in his own paper in 2006, as follows:

    “To overcome the shortage of suitable human donors for transplantation attention has recently turned to the possibility of using genetically modified pigs as a source of cells and organs. It has been suggested that such procedures might facilitate the introduction of novel retroviruses, normally resident in the pig germ line, into the human population (Stoye and Coffin, Nature Medicine 1: 1100, l995).”

  12. >I discussed the "Good Day / Bad Day" effect with
    Dr Ryll.

    He confirmed that our descriptions of this phenomenon were a perfect match.

    But when I told him what I was doing about it, he reacted with stunned disbelief.

    As did everyone else.

    I suppose that I can't blame anyone, for I can hardly believe it myself.
    It's one of those things where
    you had to be there.

  13. >P.S. Jamie, in this excellent hypothesis, don't forget the adjuvants in vaccines (squalene, aluminum, etc). They surely make things much worse, perhaps they allow greater replication of transferred virii. Adjuvants can really upregulate inflammation, and downregulate proper immunity.

  14. >adding to the mess:

    Mixed retrovirus infections.

    Mixed retrovirus infections frequently result in viral pseudotyping in which the genome of a virus is encapsulated within virions possessing a distinct host range from that encoded by the packaged genome. Pseudotyping between different classes of murine retroviruses has been extensively documented in vitro and in vivo and can result in profound changes in viral replication and pathology. A number of non-human retroviruses exhibit infectivity for various heterologous cell lines which often include human cells. Thus there is a possibility of generating heterologous mixed retroviral infections in humans upon the administration of clinical reagents developed in non-human systems. Pseudotyping between retroviruses from heterologous species (e.g., murine and primate retroviruses) has also been documented in mixed in vitro infections, as has pseudotyping between retroviruses and viruses of other families (e.g., rhabdoviruses). The effects of heterologous pseudotyping on viral replication and pathology in vivo have not been extensively studied and represent a potential concern for the development of clinical reagents in heterologous cells.
    Evans L; Dev Biol (Basel). 2001;106:181-6; discussion 253-63.

  15. >P.P.S. Jamie. So polite about coverups…which I appreciate.


    and that was strangely absent from USA press coverage.

    Accidents happen?…hmmmm….surely they can and do. How do industries maintain integrity while making a profit?

    In Eisenhower's farewell address – delivered on January 17, 1961 – e warned about the growth of a "military-industrial complex" in the United States.

    "Now, this conjunction of an immense military establishment and a large arms industry is new in the American experience. The total influence – economic, political, even spiritual -is felt in every city, every state house, every office of the Federal government. We recognize the imperative need for this development. Yet we must not fail to comprehend its grave implications. Our toil, resources and livelihood are all involved; so is the very structure of our society.

    In the councils of government, we must guard against the acquisition of unwarranted influence, whether sought or unsought, by the military-industrial complex. The potential for the disastrous rise of misplaced power exists and will persist….

    …Akin to and largely responsible for the sweeping changes in our industrial-military posture, has been the technological revolution during recent decades.

    In this revolution, research has become central; it also becomes more formalized, complex, and costly. A steadily increasing share is conducted for, by, or at the direction of, the Federal government.

    Today, the solitary inventor, tinkering in his shop, has been overshadowed by task forces of scientists, in laboratories and testing fields. In the same fashion, the free university, historically the fountainhead of free ideas and scientific discovery, has experienced a revolution in the conduct of research. Partly because of the huge costs involved, a government contract becomes virtually a substitute for intellectual curiosity. For every old blackboard there are now hundreds of new electronic computers.

    The prospect of domination of the nation's scholars by Federal employment, project allocations, and the power of money is ever present – and is gravely to be regarded."

    Check out David Noble's work, too. He is a very interesting scholar and activist.

    If you don't think vaccines are the direct consequence of the military-industrial complex…and Eisenhower was not prophetic…well…

    It's very brave of you to take on this medical conundrum *and* by implication, the military-industrial complex.

  16. >I saw this email on some forums,
    very interesting.

    As a physician investigator I try to keep an open mind to possibilities for why XMRV is being detected in some patients with CFS but not others. One possible "far out" explanation, for which I nor anyone else has data yet to support [bold in original], is that a product is being injected or infused into some patients that is contaminated with or derived from mouse cells containing XMRV or MLVs. There are unregulated products without quality controls being advertised and some of these may be used by patients with CFS who are desperate for relief from their symptoms.

    There have been several well documented instances of contamination of vaccines and medical products with transmissable agents, despite regulation and quality control procedures in place. So, the potential for this occuring with unregulated/uncontrolled products is real and should be considered.


    John W. Mellors, M.D.
    Professor of Medicine
    Chief, Division of Infectious Diseases
    University of Pittsburgh School of Medicine

  17. >

  18. >Erik, not everyone who got sick then was restricted to the sites of the most famous outbreaks. My wife got sick in 1986 with what was much later diagnosed as CFS while living in moldy, crowded, stressful San Francisco.

  19. >"The current epidemic of neuroimmune illnesses may be due to the introduction of simple retroviruses into the human population through the use of vaccines. This hypothesis needs to be studied. I am not some crazy conspiracy theorist. The pathogenesis of the illnesses needs to be further elucidated and specific treatment found. Now."

    You make an awfully abrupt leap from saying that the hypothesis should be studied to saying "the pathogenesis of the illnesses needs to be further elucidated and specific treatment found. Now." This implies that the hypothesis is true. I find this very anti-scientific.

    I agree that the hypothesis that various neuroimmune illnesses are caused by retroviruses is one that should be investigated. Also, the hypothesis that retroviruses have been introduced through vaccination should be studied. These hypotheses are independent of each other. Each would take a great deal of research and lot and lots of time to confirm. I hope that both hypotheses are already in some way under investigation. If these are plausible hypotheses, there will be scientists eager to pursue them.

    We must keep in mind that other neuroimmune illnesses, like Parkinsons or MS, are not the "orphan" illnesses that CFS is, and that extensive research is already being done on these conditions. The scientists involved in this research would surely be thrilled to find a retrovirus or to discover a link to vaccination.

    The link between autism and vaccination has been extensively studied (and most of the evidence is negative). To me, this suggests that the possible dangers of vaccination are already taken seriously by at least a subset of scientists.

    I feel so frustrated. On the one hand, the medical and journalistic establishments seem so eager to reject the XMRV hypothesis out-of-hand. And I'm not confident that other avenues of research on CFS will be opened up if this one closes down. On the other hand, activists and patients, including most folks on this blog, are so dead-set on the XRMV (or other retrovirus) hypothesis or vaccination hypothesis or other pet theories (mold, heavy metals…..) that they appear to me to be equally closed-minded. None of this encourages me to feel that ANYONE will be open-mindedly, with the true scientific spirit, trying to figure out the source(s) of this dreadful illness, which really could be anything. Anything. We don't know. And our illness could be related to lyme disease…or not. Related to MS….or not. Related to autism….or not. We don't know. And we never will know until it is simply taken seriously as an illness and given research resources. That's what we need. We need to have our illness taken seriously.

    Jumping to conclusions about its causes doesn't really help us to be taken seriously, in my opinion. In fact, I think it's deadly. I think it chases off scientists, journalists, and others that we need as allies. I am so frustrated I want to weep.

  20. >Dr Jamie, I'm excited to see you staying on this issue that I have long believed to be central in this Neuroimmune disease epidemic. It's the elephant in the living room, imo.

    What do ME/CFS, Lyme, GWS, and Autism, all have in common? They are all neuroimmune diseases with apparent similar etiologies….and all are shoved under the rug by our gov health agencies.

    Thanks for staying on this and providing some great links.


  21. >To Anonymous wanna-weep.

    Did you see my post about astrocyte depolarization?

    Ask yourself why a guy who calls himself Erikmoldwarrior would mention such a thing if he were stuck on a pet-theory of mold.

    I use the mold-factor as a test of the medical professions true interest in CFS.

    Mold was at "Ground Zero" for the creation of syndrome. which elevates its role from speculative "theory" to a bit of evidence that CFS researchers can not legitimately ignore,
    and still think of themselves as honest CFS researchers.

    Its role can be disputed, but not ignored, at least, not without casting aside objective scientific methodology… which disqualifies them from being "scientists".

    I start by passively suggesting to them that they might look into it. A request which is politely refused.
    Then I gradually increase the "amplitude", noting at each turn, that their disinterest escalates in perfect correlation to the intensity with which the request is construed.
    When their obstinate stance reaches the point of adamant refusal, it always ends up with my telling them that as as scientists, it is not up to them to bias their research by selective omission of pertinent evidence.
    They MUST at least take the mold-factor under consideration.
    At which point they turn and flee.

    Your concerns are utterly and completely warranted.

    The medical profession has shown themselve to be completely antiscientific, and only views "CFS" as a convenient vehicle to put wings on any imaginative flight of fancy they care to invent.

  22. >John Mellors has forgotten that the same stark differences in studies is also being seen in those with prostate cancer, and that in the UK, where anything but abusive "treatments" are banned, people are testing positive.

    So we have positives in a country where people with ME, yes people, won't have had these unregulated products. We have researchers that are somehow picking people who must have and must not have taken these products that they can't get, and somehow prostate cancer patients are also using these unregulated, never been named, don't know what they are products, but again researchers are managing to separate out those who have and haven't taken them, when the don't know who has, and never tried to separate them.

    Considered – it don't make sense.

  23. >It is also interesting to note how many unregulated products without quality controls are advertised on sites for Cancer, AIDS, MS, etc, who are desperate for relief from their symptoms.

  24. >What about endogenous retroviruses (Herv's) in humans recombining with animal viruses to activate Herv proteins and create disease. It makes sense to me that internal and external factors are working together to produce neuroimmune illness.

  25. >Makes sense to me, too.
    I told Dr Cheney and Dr Peterson that until they figure out the cause of CFS, I will work on the factors which I can control.
    So I did.

  26. >Calling BS on Dr. Mellors' proposal:

    "a product is being injected or infused into some patients that is contaminated with or derived from mouse cells containing XMRV or MLVs. There are unregulated products without quality controls being advertised and some of these may be used by patients with CFS who are desperate for relief from their symptoms"

    Mellors would seem to be saying XMRV comes from Myers cocktails, Mg-B12 injections, extracts, stem-cell creams, etc., from Cheney, Lapp, or numerous holistics WPI test subjects saw along the way. I.e., forget healthy controls, PC and respiratory patients: it's something benign we gave it to ourselves once already sick. That the CAA chose to bank blood from this guy is disturbing.

  27. >Unfortunately, it's more likely to be regulated products "contaminated with or derived from mouse cells containing XMRV or MLVs" being injected or infused. At least he thought of the possibility, but reached the wrong conclusion about where it probably came/is coming from.


  28. >I just want to say….
    all this is really heart breaking.
    putting all the facts together and working all this out has made me feel so sad, I feel so sad that humans have done this to one another.
    I do believe it was not done intentionally – at least at the start.
    But we must now put right all that is wrong and try and sort this mess out.
    I really hope the scientists will work to fix this and we can get treatments, move on and get well, thats all want and all we deserve.
    God bless all those who are working to find the truth.
    Love crafter Kate xxxxxxxx

  29. >Limitations of the process to remove infectious viruses from cell lines

    Note points 1.6 and 1.7 on page 3 – I could not copy and paste…

    On page 5 they say, under 3.2:
    "Results have shown that even small modifications in procedure or the particular laboratory strain of virus used can have a large effect on virus removal or inactivation"

    also note 3.5 "occasional cases have been reported" (what about unreported ones?)

    On page 6 they talk about rodent retroviruses. This guideline was written in 1994, what was the knowledge/awareness before then?

    Interesting discussion on page 9 on "Limitations of Validation Studies", i.e. numerous factors that may lead to INCORRECT ESTIMATE OF THE ABILITY OF THE PROCESS TO REMOVE NATURALLY OCCURRING VIRUS INFECTIVITY

  30. >Characterisation of endogenous retrovirus in rodent cell lines used for production of biologicals

    J. Shepherd et al, Biologicals, Volume 31, Issue 4, December 2003, Pages 251-260

    Rodent cells are used widely to manufacture recombinant proteins for pharmaceutical use in humans and animals. However, all rodent cell lines express endogenous retroviruses that require appropriate testing regimes for identification and characterisation. In this communication we report the results of transmission electron microscopy, reverse transcriptase assay and infectious virus assays for retrovirus in 185 manufacturer cell banks of mouse, rat or hamster origin. The results indicated considerable variability of retroviral expression levels by transmission electron microscopy and reverse transcriptase assay, but nevertheless characteristic features of each cell type were observed. Infectious retrovirus was detected in mouse myeloma and hybridoma cell lines, but not in cell lines of hamster or rat origin….

    Rodent cell lines have for many years been used as substrates for production of biological therapeutics such as monoclonal antibodies, recombinant proteins, vaccines and gene therapy virus vectors. It has long been recognised that such cell lines contain retrovirus elements that may be expressed as particles detectable by electron microscopy. Such particles may be infectious, as in the case of Murine leukaemia virus (MLV), or defective and non-infectious, as in the case of the Chinese hamster ovary (CHO) cell retrovirus.]. Despite the lack of evidence for an association between murine retrovirus and disease in man, the potential contamination of therapeutics with agents associated with oncogenicity and immunosuppression in therapeutic products is a cause of regulatory concern. Detection and characterisation of retrovirus in manufacturer‘s master and end of production cell banks is recommended by regulatory agencies using techniques such as electron microscopy, reverse transcriptase assay and appropriate infectivity or co-cultivation assays. In addition, determination of retrovirus particle load and experimental demonstration of appropriate removal or inactivation of retrovirus during purification is required for each product [ref: Committee for Proprietary Medicinal Products. Notes for guidance on quality of biotechnological products: viral safety evaluation of biotechnology products derived from cell lines of human or animal origin (CPMP/ICH/295/95), European Commission, Brussels (1997) – see below
    …The study indicated characteristic features of retroviral expression in each cell type tested. All RT-positive cell lines demonstrated preference for manganese-dependent RT, characteristic of the Gammaretroviridae.

  31. >Part 1 from:

    3.2.1 Tests for Retroviruses
    For the MCB and for cells cultured up to or beyond the limit of in vitro cell age used for production, tests for retroviruses, including infectivity assays in sensitive cell cultures and
    electron microscopy (EM) studies, should be carried out. If infectivity is not detected and no retrovirus or retrovirus-like particles have been observed by EM, reverse transcriptase (RT) or other appropriate assays should be performed to detect retroviruses which may be noninfectious. Induction studies have not been found to be useful.


    Case B: Where only a rodent retrovirus (or a retrovirus-like particle which is believed to be non-pathogenic, such as rodent A- and R-type particles) is present, process evaluation using a`specific "model" virus, such as a murine leukemia virus, should be performed. Purified bulk`should be tested using suitable methods having high specificity and sensitivity for the`detection of the virus in question. For marketing authorisation, data from at least 3 lots of`purified bulk at pilot-plant scale or commercial scale should be provided. Cell lines such as`CHO, C127, BHK and murine hybridoma cell lines have frequently been used as substrates`for drug production with no reported safety problems related to viral contamination of the`products. For these cell lines in which the endogenous particles have been extensively`characterised and clearance has been demonstrated (note limitations below), it is not usually necessary to assay for the`presence of the non-infectious particles in purified bulk. Studies with non-specific "model"`viruses, as in Case A, are appropriate.
    … Cell lines derived from rodents usually contain endogenous retrovirus particles or retrovirus-like particles, which may be infectious (C-type particles) or non-infectious (cytoplasmic A- and R-type particles). The capacity of the manufacturing process to remove and/or inactivate rodent retroviruses from products obtained from such cells should be determined. This may be accomplished by using a murine leukemia virus, a specific "model'' virus in the case of cells of murine origin.

  32. >Part 2 from:


    6.4 Limitations of Viral Clearance Studies
    Viral clearance studies are useful for contributing to the assurance that an acceptable level of safety in the final product is achieved but do not by themselves establish safety.Number of factors in the design and execution of viral clearance studies MAY LEAD TO AN INCORRECT ESTIMATE OF THE PROCESS TO REMOVE VIRUS INFECTIVITY. These factors include the following:

    1. Virus preparations used in clearance studies for a production process are likely to be
    produced in tissue culture. The behaviour of a tissue culture virus in a production step
    may be different from that of the native virus; for example, if native and cultured
    viruses differ in purity or degree of aggregation.
    2. Inactivation of virus infectivity frequently follows a biphasic curve in which a rapid
    initial phase is followed by a slower phase. It is possible that VIRUS ESCAPING A FIRST INACTIVATION STEP MAY BE MORE RESISTANT TO SUBSEQUENT STEPS. For example, if the
    resistant fraction takes the form of virus aggregates, infectivity may be resistant to a
    range of different chemical treatments and to heating.
    3. The ability of the overall process to remove infectivity is expressed as the sum of the logarithm of the reductions at each step. The summation of the reduction factors of multiple steps, particularly of steps with little reduction (e.g., below 1 log10), MAY OVERESTIMATE THE TRUE POTENTIAL FOR VIRUS ELIMINATION. Furthermore, reduction values achieved by repetition of identical or near identical procedures should not be included unless justified.
    4. The expression of reduction factors as logarithmic reductions in titer implies that, while residual virus infectivity may be greatly reduced, IT WILL BE NEVER REDUCED TO ZERO.
    For example, a reduction in the infectivity of a preparation containing 8 log10 infectious units per ml by a factor of 8 log10 leaves zero log10 per ml or one infectious unit per ml, taking into consideration the limit of detection of the assay.
    5. Pilot-plant scale processing may differ from commercial-scale processing despite care taken to design the scaled-down process.
    6. Addition of individual virus reduction factors resulting from similar inactivation mechanisms along the manufacturing process may MAY OVERESTIMATE OVERALL VIRAL CLEARANCE.


    states the following:

    … Validation studies are complex.and expensive and a clear position on this is important. The extent to which manufacturers are able to refer to in-house experience concerning virus safety evaluation. For such cases, the virus safety of a given cell culture system and/or the capacity of established manufacturing process steps to inactivate/remove potential virus contaminants may have been demonstrated with several previously developed products. Such a database may serve as supportive data to JUSTIFY A REDUCED VIRUS SAFETY EVALUATION PROGRAM FOR NEW PRODUCTS THAT ENTER DEVELOPMENT.

  34. >There is yet more, unfortunately …

    Re retroviral contamination of chicken embryo-grown products there were a few studies in the late 90s indicating that there may be a problem. Have a look at this one by the Swiss group

    … read the first and second paragraphs of discussion. They detected RT activity in all vaccines, but WHO experts concluded that it poses no danger to humans (!!!!!!!!!!). Then in the next sentence we find out that they haven't a faintest clue what causes that RT activity. But they do suspect retroviruses are involved (!!!!!!!!!). No worries then.

    Shortly (very shortly!) after that study there were 3 negative studies, 2 done by CDC, and 1 by FDA, saying there is no problem with retro contamination, everything is hunky dory, nothing to see, go home, book is closed.

    case closed!

    BUT THEN this one comes along in 2008:

    Molecular characterization of three recombinant isolates of avian leukosis virus obtained from contaminated Marek's disease vaccines.

    Three natural recombinant avian leukosis viruses (ALV; PDRC-1039, PDRC-3246, and PDRC-3249) expressing a subgroup A gp85 envelope protein and containing long terminal repeats (LTR) of endogenous ALV-E viruses were isolated from contaminated commercial Marek's disease vaccines, cloned, and completely sequenced. Their full genomes were analyzed and compared with representative strains of ALV. The proviral DNA of all three isolates displayed 99.3% identity to each other, suggesting a possible common ancestor, even though the contaminating viruses were obtained from three separate vaccine serials produced by two different vaccine manufacturing companies. The contaminating viruses have a genetic organization typical of replication-competent alpharetroviruses. The proviral genomes of PDRC-1039 and PDRC-3246 are 7497 bp long, and the PDRC-3249 is three base pairs shorter because of a deletion of a threonine residue within the gp85 coding region. The LTR, gag, pol, and the transmembrane (TM) region (gp37) of the env gene of all three viruses displayed high identity to endogenous counterpart sequences (>98%). Only the surface (SU) region (gp85) of the env gene displayed high identity with exogenous ALV-A (98.7%). Locus-specific polymerase chain reaction (PCR) analysis for ALV endogenous sequences (ev loci) in the chicken embryo fibroblasts used to produce the original vaccine vials identified the presence of ev-1, ev-2, ev-3, ev-4, and ev-6 in all three vaccines. Homologous recombination most likely took place to involve the SU region of the env gene because the recombinant viruses only differ in this particular region from the consensus ALV-E. These results suggest that the contaminating ALV isolates PROBABLY EMERGED BY RECOMBINATION OF ALV-A WITH ENDOGENOUS VIRUS SEQUENCES before vaccine preparation. Barbosa T, et al Avian Dis. 2008 Jun;52(2):245-52.

    Can we sleep soundly as WHO says we should. Or toss and turn and reopen the book?

    Could these be the same lab/s that were involved with De Freita’s follow up research, those that could not find anything: HIV and Retrovirology Branch, Division of AIDS, STD, and TB Laboratory Research, Centers for Disease Control (Switzer and Heinene in particular)?

  35. >Anonymous of March 19, 2011 9:16 PM:

    Yours is a well-made comment.

    I think if everyone can manage to stay moderate, there is more benefit than harm that comes from people plugging away on their perspective of what might be awry with at least some of us, or our environment.

    I’m half a world away from the US in Australia, and I’ve focussed much more on trying to figure out what’s wrong with me (as opposed to what causes the vaguely defined condition ‘ME’/CFS), so I don’t have a good grasp of much of the history of the various outbreaks of ME in the US, or of individual’s stories.
    Take ErikMoldWarrior as an example. I gather he is fairly highly functional, so long as he maintains strict adherence to an avoidance-of-irritants protocol (apologies to Erik if this “gather” of mine is complete BS, if it is I’m sure Erik will correct the record). Lisa Petrison also seems to have some (personal?) reason to strongly believe in the mould factor.
    So they have good reason to plug away at the idea that mould or other toxic agent/s (flame retardant?) in the environment could trigger/aggravate ME or impede recovery.

    Jamie is rather between a rock and a hard place with this blog, which started out 100% personal, but has morphed into an important hub for information and exchange of ideas. She has knowledge and skills to produce better quality information than we’ve had access to, probably ever. She also has her pet theory.

    I share your concern for where ME/CFS research heads from here. No matter what our opinion of WPI, or of XMRV, no one can deny WPI’s achievement in putting some oxygen into the ME/CFS debate.
    Take Dr Alter’s comment from late 2010 (c & p from pugilator’s blog):
    “I’m not a CFS Dr, but have learned a lot in last 6 months. I am absolutely convinced when you define this (ME/CFS) by proper criteria, it’s a very serious, medical disease. Characteristics of a viral disease. If it’s not XMRV, we must continue the research to find out what is”

    We have their attention!

    Our task is to maintain their attention and feed them good quality information that might contribute to a “That’s funny …” moment.

    Also from pugilator’s blog comes this quote:

    The most exciting phrase to hear in science,
    the one that heralds the most discoveries,
    is not “Eureka!” (I found it!) but “That’s funny…”
    Isaac Asimov

    I think we need to push for more stringent diagnostic criteria and emphatically condemn self-diagnosis. In Australia, pretty much half the population seems to think they have or know someone with CFS. Just a few days ago an acquaintance told me that her 70 something y.o. partner has CFS. She thinks he has unrealistic expectation of what he can do without tiring (e.g. playing 7 rounds of golf in one week is overdoing it in her opinion!), but she still publically states that he has CFS.

    Take a look at what has come from one Parkinson’s patient getting across his experience to a disbelieving doctor (the “stunned professor Bloem”, who subsequently stated, “… I think what we as doctors should do much more is listen to our patients and explore the unique opportunities that patients have found themselves …”)

    Praise be to that idea.

  36. >Thank you again Dr.Deckoff-Jones. This theory makes perfect sense to me. What a journey this has been. First they tell me that my illness is psychological – I disprove this by providing a whole host of test results which suggest many biological abnormalities. Then they tell me that I will recover in 2 years – I disprove this because I have been ill for over 4 years now.
    They then tell me that XMRV doesn't exist in Europe – I disprove this by testing positive by serology (I live in the UK).
    They then tell me that XMRV is only a contaminant – I can't disprove this but the WPI and this blog will.
    This is going to be a long,hard slog but you are getting there and I am more grateful than you will ever know. The evidence is out there and it cannot be dismissed any longer – I will not be dismissed any longer.
    Change is coming, slowly but surely.
    I'm sorry I can't contribute to these responses in a more scientific way but I am the human element on the other side of all of this science and I am just watching and waiting!!

  37. >Jayne, yes. You have it exactly right.
    Moderate attempts at avoidance of biotoxins left me spiralling into deeper illness.
    I hit a crisis point in 1994 and was forced to abandon my efforts to have a normal life.

    By shifting my perspective from conceptualizing irritant-exposure in terms of dosage, to one of relying on my indicators of autonomic dysfunction and capillary hypoperfusion as guides to just how extreme my avoidance strategy must be, to work my way around unbelievably small amounts of these ubiquitous environmental substances, I was able to turn my situation around and recover in a fairly dramatic fashion.

    It had been my impression that CFS researchers were looking for possible clues about etiology, and CFS patients were in search of "Anything that helps"

    This one, along with a few others, seemed to qualify.

  38. >This is the only scientific theory I've heard that explains all of the science AND the politics. Everything fits so well – it's hard to believe that this is not the right solution.

  39. >I am "wanna-weep Anonymous", as ErikMoldWarrior says. Thanks, Jayne, for a very insightful contribution to the discussion. I strongly agree with your point that strict diagnostic criteria are very important now. I like the Canadian definition, but that may just be because "PEM" (so called) is my weirdest and most disabling symptom.

    To me, it seems that we all need to be more humble about just how representative our own experience of (and theory about) CFS is. For example, I have terrible OI and PEM, but that doesn't necessarily mean that those are the defining characteristics for everyone. Erik, you have extreme sensitivity to some environmental contaminants, but that doesn't mean everyone with CFS shares this. You think that this is the ultimate clue. Maybe. Or you think it is a clue scientists must take seriously to be good scientists. Maybe.

    I love Jayne's quote from Asimov about the "That's funny…" moment. I think that's very true, and the doctors and scientists who listen very closely to patients' stories are the ones who are most likely to make the connections that solve the puzzle.

    The problem for scientists and doctors is that many many people have different convictions about what triggered their illness or what sustains it or what helps them improve. If you have (as a CFS specialist will have) hundreds of people walk (or roll) through your door with this devastating illness, you will hear hundreds of different theories and clues about it. They won't match up at all. It's the same with many illnesses.

    For example, if you take mothers of children with asthma, you will find that many of them have definite notions of what contributed to their child's condition, what first triggered it, what makes it worse, what helps it. Some of them will be right (at least for their child), but many of them will turn out to be putting 2 and 2 together and getting 5. Some of them will be excellent detectives and observers, but others will be people just wedded to a pet theory. How are doctors/scientists supposed to know who is who and what is what?

    Erik may be a deluded crackpot (sorry Erik, not what I really think), or he may be right for him and wrong for me, or he may be the great observer and detective that everyone should have been listening to all along. But how is a doctor or scientist supposed to know which?

    I'm not sure just what I'm trying to say here, but I guess the heart of it is that, although we mustn't have humility about the seriousness of our condition, or about our right to be attended to by the scientific and medical establishment, I think we need to have humility about our own perspectives on the disease.

    If, for example, the mystery of CFS is solved, but it turns out that the solution doesn't work for me, or for you, because it turns out we had something different from most other people all along, well, that's not going to be easy to accept or live with, but it won't mean that the solution is BS.

    If we have a pet theory of our illness, and it is proven over time to be wrong, will we listen to that proof? Or will we dig in our heels and insist that the proof is an illusion? Arrogance will lead us in one direction, humility in another.

    Erik, I am glad that you have found an approach that keeps you relatively well. Can you share in detail what that approach is? I am always interested to at least consider what works for other CFSers. For me, so far, the key to being able to function the best I can is to pace extremely carefully, spend a lot of time horizontal, and avoid PEM, because my capacity expands gradually if I don't blow it. That is just disease management, I know, and isn't addressing the causes or sources, but it's the only thing I know that helps me live as fully as possible.

    So today, I don't wanna weep, I just want to hear more open-mindedness about CFS, here and everywhere else.

  40. >Questions for Lisa Petrison & Eric MoldWarrior

    As both of you seem to be considerably improved,
    could you please address the specific methods
    both of you used in gaining such improvement.

    Also, how ill were you before you began your
    journey toward improvement?

    Thank you for your replies.


  41. >Gretchen.
    For brevity, I'm a survivor of the Incline Village incident described in Osler's Web.
    The book is 100% accurate. The mystery illness is exactly as described.

    The important part for our purposes here, is Dr Cheney's observation that having once been triggered, unknown factors seem to move in, keeping the illness-process unrestrained and progressive.
    Dr Cheney likened it to a landslide started by a small stone. "Never give up the search for the bug", but at the same time, explore the
    co-factors which appear to be perpetuating the process.
    I stumbled right over one that seemed worthy of further investigation.
    The more I compared my situation against others, the plainer it seemed that a great many of us were in thrall of this bizarre "effect".
    Assigning a precise "cause" or specific value to this effect always causes instant dismissal,
    for no such effect is recognized in medical tomes, although hints of its mysterious presence do appear in vague references; Never-explained.
    Like CFS itself, this effect is such an enigma that the best way to confront the unusual nature of this situation is by direct experience.
    I lead CFS patients to a place that is rife with the effect, so they can feel it for themselves.
    "Avoid it as if it were plutonium", and see what happens.

    Yes, I realize this sounds rather cryptic, but isn't that how all new paradigms are?
    Imagine trying to explain electricity to a tribal member from the deepest Amazon jungle who has never seen it.

    One zap equals a million words.

  42. >In the trailer for the What About ME documentary film, you can see my puzzlement that some people weren't recovering, they were even getting WORSE.

    Was there a pattern to this?
    What, if anything… could be done about it?

  43. >Eric,
    I apppreciate your prompt reply. I own an
    apartment in a high rise building that is filled
    with very high levels of mold.

    Stachybotrys: spore count 11,700
    Aspergillus/Pen. spore count 11,550
    Cladosporium spore count 9,510
    On and on with some 15 molds found.

    These molds have permeated every room in my
    apartment. It was supposedly remediated after
    Hurricane Ike, but I just had this independent
    analysis done and find that the mold has
    returned more vehemently.

    I am so very sick that I wonder if I have the
    strength to make a move, but feel I will die
    if I stay here.

    Should I just evacuate with only the clothes
    on my back? What would be your suggestion??

    I don't really trust another try at remediation
    as I believe the whole building is contaminated.

    Your reply will be appreciated.


  44. >Gretchen, I would leave the clothes,
    and take nothing, not even a toothbrush.
    I would leave immediately.

    That was the wise advice Dr Herman gave to the Porath family:

    The Fire Cure.,,20134855,00.html

    The Porath's had family come with new clothing. They changed their clothes on the front lawn to prevent contaminating the car.
    My mother met the Porath family and after hearing their story, told me "It is just as you said, it is EVERYTHING you said".

    I wish it wasn't, but it is.

  45. >I wasn't going to go into "the effect" so soon, but what the heck?

    Here is another horror story about "clothes on your back" type evacuation.
    Moms Against Mold:

    Now, ask yourself this.
    What happens to Stachy-slammed possessions that come out of a badzone?
    Does it all wind up in a dumpster and cease to be a problem?
    No.. some of it goes somewhere else.

    And where-ever it goes… there you will find the "effect".

  46. >So if xmrv or mlv came in vaccines.

    did HIV come from the hep B vaccine in the 1970s?

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