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Graham McPhee spells out some of the cold, hard facts about the dismal state of ME research and politics, and has some suggestions as to what we can do about it ...
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The real story about XMRV coming out today?

Discussion in 'XMRV Research and Replication Studies' started by VillageLife, Sep 23, 2011.

  1. In Vitro Infidelium

    In Vitro Infidelium Guest

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    One can come up with ever more sophisticated propositions, but the question in science is whether these propositions are independently testable. Gender differences resulting from sexual transmission is just a variation in exposure - it was precisely the point I made in response to Redo rgarding HIV - in the 1980s and 90s in the US, gay men were identified as especially prone - from the late 1990s onwards it's been recognised that women in developing countries are at higher risk. In neither case was/is HIV making a choice about who to infect - it's simply a matter of exposure. Unless a pathogen is ubiquitous, patterns of exposure are easily identifiable - where are the patterns in M.E/CFS ? It doesn't affect any given geographical area with any consistency, it has no social or cultural preference, and apart from a certain age disaprity, in rather the wrong direction (cf. adolescent diseases -HIB, EBV etc) the only notable demograhic charateristic is the gender differential. Of course there may be hidden epidemiological issues - but we have to progress from what we know, not from what maybe.

    The value of an hypothesis is whether or not it is testable - simply coming up with a list of things that help lever a proposition into a conception that fits a preferred perspective will not produce a testable hypothesis. HGRVs are no doubt very worthy of scientific enquiry, what no one has at present is any testable hypothesis about why any given HGRV should be associated with M.E/CFS any more than any other pathogen. There is no basis therefore to make a choice of what to look for or why ? Or even what it might possibly mean when you find what you are looking for. The whole XMRV fiasco (OK it was a great reminder to researchers that they need to be careful when arriving at conclusions - prior plausibility rules !) has not even come close to even asking the question about disease causation - all that time, all that expense and it was just a fishing trip. How many more blind fishing trips will this kind of approach take to come up with something useful ? Monkeys, typewriters, the works of Shakespear and an infinte amount of time, suggest themelves as some how relevant.

    IVI
     
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  2. SilverbladeTE

    SilverbladeTE Senior Member

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    IVF
    well, you can argue that ME is more important to treat, because the victims live so long they cost a vast amount of resources, lost working time etc.
    And since the cause is not known, and thus it's transmissibility, lethality etc, it's PARAMOUNT to find it, ASAP.

    For all you know, the cause of ME maybe a virus that's responsible for much of the autoimmune/cancer deaths in the world.
    Or it could be incredibly infectious and affect folk in different ways thus no one has linked it to a common cause.

    HIV is udnerstood, treatment available, long term, vaccines or cures are thus possible and being worked on
    NOTHING WHAT SO EVER is being truly worked on for ME, because we have no clue as to a true, clear cause and thus, proper research on treatments.

    That's the real job of Science: exploring and understanding the unknown. Not prostituting itself for power and money.
     
  3. In Vitro Infidelium

    In Vitro Infidelium Guest

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    What model ? There is no model of HGRV relevance to M.E/CFS. Lombardi et al simply carried out a speculative study looking for a novel (possibly non existent outside of contiminated reagents) RV, there was no sound reasoning why such an agent - it had no known pathogenic attributes - would have any relatonship to M.E/CFS. The only relationship now is that Lombardi et al simply carried out a speculative study looking for a novel (possibly non existent outside of contiminated reagents) RV in M.E/CFS patients: circle closed.

    The lack of any clear disease model is of concern - but shows where research is needed, especially in epidemiology, science needs to understand far better who has M.E/CFS and how the illness affects them relative to age, gender and variables such illness exposure, genetic profile etc. From this perspective the approach of the Chronic Fatigue Initiative looks extremely promising, as so long as the CFI can promote co-operation with other research groups, then we may actually be witnessing a game changing development.

    IVI
     
  4. Bob

    Bob

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    You have highlighted some weaknesses in the first reason that I gave, but the second possible reason that I gave for gender differences is stronger, and you have managed to ignore that.

    If a virus has been found in 85% of ME patients, and only 5% of healthy controls, then the need for a disease model goes out of the window... It obviously needs further investigation based on those results alone...

    Like you say, large scale epidemiology studies just haven't been carried out... But that doesn't mean that we should halt all other speculative research.

    A virus would fit ME very well... I have already given reasons why there could be gender differences... There doesn't need to be other population differences... I think that flu affects everybody more or less equally, as long as people are exposed to other people, then they risk getting flu.

    But I do agree that it would be nice to have more research, such that we understand exactly how ME is distributed through the population, and what the risk factors are. But everytime they do that sort of study, they decide that it's all due to childhood trauma, and thus a psychiatric disease. So I don't think I would advocate for epidemiological studies over the other work that is currently being done with immune systems, biomarkers etc.
     
  5. Esther12

    Esther12 Senior Member

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    I don't really understand this point either. Especially with a new virus, which we do not really understand, associated with an illness like CFS, which we do not really understand. When the WPI started talking about 95% of patients being positive, that seemed strange, but the initial finding of 65% in CFS patients and 7% in controls could have been explained in all manner of different ways. It now looks like those figures were wrong anyway, but I don't think we have compelling evidence about the nature of CFS which could have allowed us to know they were wrong prior to replication attempts.

    Given what a mess CFS research is, having a quick look in patients for any new pathogen that comes along seems like a worthwhile thing to do.
     
  6. Bob

    Bob

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    Well I've never before heard an ME patient saying that more money should be devoted to HIV than to ME. Even if any ME patients have given it any thought, I can't see anyone writing such a letter to their political representatives.


    Humans make value judgements all their lives, and science is not immune from these value judgements.

    How do we prioritise what should be researched and what isn't important to research?

    It's all based on value judgements, and these are based on emotions, culture, history, what we perceive as fairness, economics etc etc etc.

    As an example, we could devote all of our scientific resources towards eradicating all diseases in birds.

    But we don't. We devote most of our resources to diseases in humans.

    Why? Why are humans valued over birds?

    It's an emotional and cultural response. We simply have more empathy for humans, and value humans more (as a society - i can't speak for individuals).

    So of course you have to make value judgements in science.


    Emotional appeals to justice do indeed bring progress. This has happened throughout history.
    Our lives are based on emotions, and it is emotions that make the world go around, figuratively speaking.
    Most positive cultural changes in history come about through emotional appeals to fairness and justice.

    As for your 'philosophical perspective', I believe it is flawed, precisely because it fails to take into account the personal experiences of patients.
    Wessely has a dogmatic philosophical perspective, and he fails to listen to his patients, he fails to have empathy for ME patients, and he fails to take into account his patients' personal experiences when formulating his theories and therapies.
    Thus, his approach to medicine becomes abusive, harmful and deeply innappropriate.
    I'm not comparing you to Wessely, but I'm pointing out the dangers of dismissing people's personal experiences, whilst placing your own (flawed) philosophical musings onto a pedastal, and ignoring the realities of people's lives.

    As for 'survival in the face of adversity', that's very easy to say
     
  7. alex3619

    alex3619 Senior Member

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    Hi, on science and cultural values, lets look at war for comparison. War is best left to generals without interference from politicians, but politicians have to select goals and values, and have to supply funding.

    Science is no different. Science is best left to scientists (but some doing research in the medical profession do not have good research training in my opinion and so are dubious scientists at best); the decision as to what to study, in what order, with what funding, is in the realm of politics. Its not up to scientists at all.

    We are stakeholders in the politics of ME funding and research direction. It is not only our entitlement, it is our duty to ourselves and other patients to be involved in the debate on research direction. It does not matter if we get it wrong either - if only people who were right all the time were allowed to vote or stand for public office all democracies would fail.

    The essence of good democracy is an informed public. The essence of an effective ME community is an informed ME comunity.

    I have been thinking about why so many have been strongly pro-XMRV. One possible reason is this: it offers a potential explanation that is provable or disprovable, a single potential causal mechanism. Most of the other hypotheses out there are more complex in many ways.

    Peronally a retrovirus, or other stealth virus, fits the two major ME hypotheses very well, even if its not directly causal. The two hypotheses are that it is caused by an unidentified virus, the second that viral or other stressor such as toxins induces a change in the immune system that does not switch off. Various biochemical mechanisms may or may not be causal here, such as oxidative and nitrosative stress or glutathione depletion.

    I have long had the suspicion that ME is induced by many different pathogens, that it is an emergency antiviral defence mechanism induced when secondary evidence for a viral assault on critical systems in the body is detected, such as heart or brain or spine. If the body reacts to this as though a virus, even though it could be a toxin in some cases, and it doesn't resolve, there is no reason they body should stop fighting. It is reacting to a life threatening pathophysiology, it can't tell what the cause is, its just stimulus-response. The emergency mechanism includes producing elastase and triggering the cleavage of ribonuclease L into the 37 kilodalton form along with associated bioactive molecules that impede metabolism, thus slowing potential viral replication - and our metabolic rate as well.

    Now high levels of non-replicating viruses could be causing this such as herpes and enteroviruses, which is a common tissue finding in ME. However, a low copy number retrovirus fits this as well, even if its not particularly pathogenic.

    The mechanism does not switch off because it fails to reverse the signals that are telling it to continue. Non-replicating or slow replicating viruses could do this if the cells that are infected are not destroyed. Given that up to half of the cell in our guts contain enteroviruses in most patients, it is patently obvious that we cannot kill all the cells involved, the body has to find another way to fight it. By attacking the gut it is quite possible that the level of damage induces counter-mechanisms to slow or halt some antiviral function.

    As for MLV pathology in mammals, it clearly causes the same kinds of cancers found commonly in ME and also neurological damage. MLVs are a good candidate - but this does require clear and unambigous evidence of MLV-related infection which we do not have to date. I also would not rule out other non-MLV retroviruses at this stage.

    This is just one possibility to show it does not have to be either a virus or an aberrant immune response, it can be both.

    Of course I have not mentioned the other major hypothesis, neurological damage. I don't know enough about neuroscience, despite having studied some neuroscience, to produce a coherent model. Perhaps the kindling model is a good one here?

    Bye
    Alex
     
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  8. eric_s

    eric_s Senior Member

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    I totally agree with this. And probably, in my opinion, even more so to try to make sure enough high quality research even happens.
     
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  9. ukxmrv

    ukxmrv Senior Member

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    IVI you said

    (start)

    Differently from patiients , ALL patients ? I claim to be an affected by M.E/CFS does having a differing opinion exclude me (and indeed others who arent vocal) from an M.E/CFS diagnosis ? In any any event argumentum ad populi is hardly a basis for approaching a discussion on science.

    (end)

    You once again claim to be talking about "science" but you aren't. Once again you are merely stating your opinion, It is your opinion about HIV and the relative merits with fast/slow approaches to money, treatment etc.

    Most of your posts are about your opinion not science. If you want to talk about science that's fine but then don't fill your posts with opinion, after opinion and then complain that you are discussing science - because you largely don't.

    You may have an opinon about HIV and how it related to CFS and how much funding there should be but it's only one person's opinion. I'm happy to hear you opinion but don't get that mixed up with science and facts.
     
  10. xrayspex

    xrayspex Senior Member

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    Nice post Alex.

    I saw the abstract here of Jason's kindling model for m.e. that is interesting. the part that puzzles me tho is that a friend of mine is currently in school getting her m.a. in counseling psychology, her new found passion is learning more about "brainspotting" a therapy that addresses kindling issues, ie in truama where people have hyper arousal, she has seen demonstrations on video of this therapy where they are addressing the kindling that a war vet might get related to injury and ptsd etc So if this theory is pushed could treatment move away from antivirals to the therapist's office again? I certainly have mixed feelings about that, but I guess I could see a therapy like brainspotting used as an adjunct to other real biomedical approaches, and only if they start using that sort of approach for lots of illnesses that have a kindling component to them and don't discrimnate. Kindling and brainspotting theory acknowledge that the unwanted brain and body response is real and not just in someone's head, but uses a technique to change the brain that would induce natural healing. I know that L. Jason supports a biomedical disease model for m.e. and so I was surprised to see that word "kindling" as I associate it with my friend in grad school for psychology.
     
  11. redo

    redo Senior Member

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    Your postings on this forum is appreciated IVI. It's good for balance, and it gives us a more healthy debate. I answered your post below.

    Well, as they say, a day without learning is a day without living :Retro wink:. There are physiologically notable differences. A healthy woman has eight times higher risk of getting HIV from having sex with a man who's got it, than the other way around (PubMed ID 9270414 if you're curious). When we have no idea about how gammaretroviruses are transmitted (and even if they are an issue), it would be impossible to tell if doing this or that makes one more prone to infection.

    The point I was making was that no one knew what caused AIDS, and the fact that they didn't have a model to explain why this and that about prevalence (beforehand) didn't stop them for looking for a pathogen. And neither should it (of course - and I know you agree). What I was getting from your post, was that you thought that there ought to be a model for this before they were allowed to look for viruses in CFS patients (ethics committees can decide that, I guess you know that since you're probably a scientist yourself).

    I agree! Afterwards, it's possible to know. Beforehand it would just be speculation. Is it transmission, how the immune system works, or a thousand other possible reasons (if retroviruses is a major player in CFS). Sure a hypothesis could be useful, but I don't think it should be a prerequisite.

    HIV before the tests and ARVs came along was gravely serious, and did deserve all the attention and funding it got. But one doesn't exclude the other. If we look at US figures, on the top year 0,04 million people died of AIDS. Right now there are around 1 million people with CFS in the US, and growing rapidly (not sure if it grows more rapidly than HIV did, but it wouldn't surprise me). For many, the fatigue is just peanuts compared with the brain fog (porridge brain), visual disturbances and unbearable pain. One of the most common causes for death for CFS patients is that they simply can't bear the torture-like symptoms anymore, and decides to end it. I call that an emergency. The emergency is not because they are ending their lives in such great numbers, but because the symptoms are so impossible to live with, that many find that the rational thing to do. Speaking for myself I'd rather have lung cancer, with a slight possibility of making it, than the disease I am having now. No doubt. But the group is diverse. Some got it mildly. Sort of like a constant hangover, and are doing more or less fine. And many are somewhere in the middle.

    Not only the severety of the disease calls for instant action, but also the growing numbers. CFS wasn't such a big problem 50 years ago. It's a disease which seems to be spreading more and more rapidly.

    I agree 100% with the first sentence. But I think you're being a bit inconsistant with the last. In post #93, you write that you think the gender differencial in CFS needs rigorous testing, given the likelihood of a diagnostic bias. And now you place such importance to the unsure research on it that 'it's a huge deal'. Personally I think the gender prevalence can be anything from 50/50 to 70/30 (tops!). Most likely somewhere in the middle. But it's so uncertain, that I can't tell. Given the uncertainty it could very well be that it indeed is a fifty/fifty split. And what good would it than be to build a hypothesis (which would be much speculation, since little is known about transmission, immune response etc) when we don't even know for sure that there are significant gender differences?
     
  12. asleep

    asleep Senior Member

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    Good points Alex.

    As for why people have pushed so vigorously for examination of HGRVs, I can give my own reasons:

    You say that HGRVs offer "a potential explanation that is provable or disprovable." Indeed I think that HGRVs provide a very powerful and holistic potential explanation that fits most observations about ME like a glove. Obviously such evidence is second-order, but if you find enough evidence that there is a duck around -- duck droppings, duck feathers, duck prints, duck sounds -- it's pretty reasonable to think there might just in fact be a duck about.

    • As you mention, MLVs induce similar cancers and neurological disease in animals.
    • MLVs also induce an abnormal cytokine signature similar to that seen in ME. This signature could comprise the very "change in the immune system that does not switch off."
    • Commonly (but not consistently) seen secondary infections (EBV, HHV6, enteroviruses, etc) fit the HGRV model well, both as potential onset triggers as well as opportunistic reactivations in a chronically HGRV-impaired immune environment.
    • Retroviruses frequently induce mitochondrial damage and oxidation.
    • HGRVs as a root cause could explain the divergent onset patterns via a "two-hit" mechanism. Rapid onset happens if latent, unnoticed HGRV infection is activated due to acute immune activity (infection, trauma, etc), while gradual onset reflects the long-term damage from latent HGRV infection (neurological damage from ENV protein, long-term cellular pathology).
    • The tendency shown in the macaque study for HGRVs to retreat to tissue-tropic latency provides potential explanatory power of the relapsing nature of ME: over time, the immune system could fight the infection back into latency, only for it to come roaring back from its reservoirs under certain conditions (hormonal stressors, infection-based immune activation).
    • The recent study showing "Trojan horse" potential of HGRVs to invade the brain via T-cells and potentially induce the types of neurological damage seen in SPECT scans and other findings (glial cell activation).
    • Then there's the unnervingly bizarre behavior demonstrated by the scientific community for the past two years in response to Lombardi et al. At a minimum, it can be said that the WPI was given no monetary or collaborative support to help flesh out their findings. The response from a vocal and financially empowered segment of the scientific community seems to have been little more than an aggressive attempt to discredit and disprove (not understand and confirm). It's very hard to understand these actions as anything close to resembling genuine, objective pursuit of the truth. But then the question is, why strike out so lavishly against the HGRV hypothesis?

    To me, the notion of an "immune system that does not switch off" (without concrete explanation for why it won't shut off) falls into the class of "non-explanation" explanations, similar to "genetics" and "autoimmune." What I mean is that these "explanations" are often marched out as the "cause" of some idiopathic disease, yet they don't actually explain anything. They merely punt any hope of concrete causal understanding further down the political road by wrapping our lack of knowledge in a shiny new word that distracts the majority of the populace.

    Take, for example, "genetics" which is a go-to explanation for many of the rapidly growing, poorly understood diseases of the past couple decades (autism being a major example). It seems logically implausible that genetics could have much of any causal role in diseases that have seen an explosion of incidence within a single generation. There is simply no way a common, novel genetic factor could arise in numerous independent hereditary lines within a single generation. This is not how genetics works. The only thing that can explain such rapid increase in incidence is a novel environmental factor, most likely a novel disease agent (virus, bacteria, etc) which could induce the observed genetic alterations (retrovirus anyone?). So, in essence, the "genetics" explanation is not even consistent with the most basic incidence data for the diseases it's put forth for.

    Similarly, for "autoimmune" and "chronic immune activation." The obvious question in both cases (that is rarely if ever explored): Why, all of a sudden, have the immune systems of so many unrelated individuals across the world gone haywire in apparently consistent ways? It's hard to imagine an explanation for this that doesn't revolve around a novel environmental factor. Yet once these labels are slapped on a disease, the search for this underlying cause dries up in favor of the politically and scientifically innocuous pursuit of better understanding this labeled downstream effect.

    So, in summary, it seems to me that the leading alternative explanations for ME (as well as other similarly misunderstood diseases) are really just political proxies for the true underlying cause. The political powers can pour endless amounts of money into studying how these proxy effects happen (instead of why they happen) without there ever being any danger of uncovering inconvenient truths or costly pathogens. Cue CDC/MRC/CAA/Pandora/CFI-sponsored research into a multitude of downstream effects with no hope of rooting out the actual underlying cause.
     
  13. redo

    redo Senior Member

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    It's kind of fascinating with the "not so important because people doesn't die" argument (not talking about IVI here, just the argument in general). The argument is really based on a feeling that humans live forever. For many people, their first thought is that if 30 people lose 30 years, than that's less severe than one death. Because the 30 people will live, the other person not. But the fact is that losing 30 years is the same as losing 1/3 of a life. Simple as that. And we're all dead in the long run. If I had the option between spending 50 years in CFS-torture, and than die (we all do), or just die right away, I'd choose the last.

    But this is really off topic. It thought it fit to the losing half your life can't be compared with dying stuff...
     
  14. Bob

    Bob

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    I think that we as a community, need to be careful that we don't start making any value comparisons between the lives of ME patients and AIDS patients.

    Every person, every life, and every patient is equally important and valuable.

    I think it's more helpful to focus on our own disease, and push for more funding for that.
     
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  15. redo

    redo Senior Member

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    I have only read a couple of posts from IVI (mostly those between me and him/her) so I haven't read those you are referring to Bob (I don't read much now on the account of my health). I haven't read the whole of this thread, nor the whole of the other thread I was debating with him/her on. About the AIDS/CFS stuff, if it was me you where referring to, I wrote that "But one doesn't exclude the other" - and what I meant was that the severity of one disease doesn't exclude the severity of another. If one disease got figured out in the 80s because it simply was an emergency, that doesn't exclude that immediate action is required now. CFS is more prevalent than HIV in the 80s and 90s, more people died direct deaths from HIV in the 80s and 90s, anyways none of those is written as this or that is more or less serious than the other, it simply means it's important to figure out. It's good that you pointed it out Bob, as I can see it's easy to read me that way. :Retro smile:

    The reason why I underline that I appreciate the dissenting voices is pretty much reflections after reading this thread XMRV Article in Chicago Tribune and other papers, where Mr.Kite was pretty alone and there was a storm against him. Meeting arguments with arguments doesn't always happen when there's one against everyone.

    I haven't read those posts you are referring to, so I hadn't made up an opinion about that before posting... I've only read IVI and me. Of course, I agree it's way out of line to be disrespectful to someone who has lost a loved one.

    If it was me you mostly had in mind, than I can't say I wondered, because I haven't read it. :Retro tongue: I hope you didn't think me writing I appreciated his post was some reply to something you've written (I like your posts, it's just that I don't have the health to browse through the whole thread now to find it).
     
  16. alex3619

    alex3619 Senior Member

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    Hi asleep, in response to your post 122 I agree with most of your points. Even several years ago if I were going to write up a list of properties I would look for in a virus that can cause ME, it would be very similar to an MLV. I agree its a perfect candidate. The fit was so close I was very taken by the entire Lombardi paper within minutes of reading it, and have been all along. Bye, Alex
     
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  17. currer

    currer Senior Member

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    HGRVs are responsible for the unexplained growth in some cancers since the sixties. (So this is not only ME we are talking about here)

    No-one has been able to provide a scientific reason for the 50% growth in breast cancer cases, the tripling of prostate cancer in all age groups and the doubling of leukemia cases.

    It could be that HGRVs spreading disregarded through the population are an underlying cause of this unexplained rise in cancer.

    I would say the researcher who discovers a single cause to explain these disparate facts and resolve the problem would be in line for a Nobel prize.
    A good reason to continue, wouldn't you say?

    I wouldn't be too keen on shutting down research
    Many more people than you would think might suffer.
     
  18. currer

    currer Senior Member

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    On the subject of sex differential in disease there are differences according to sex for almost every disease.

    For example bowel cancer is more common in men.
     
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  19. RustyJ

    RustyJ Contaminated Cell Line 'RustyJ'

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    Don't buy all the hype that HGRVs are dead in the water. The scientific argument for continuing research into HGRV's: The negative studies mostly focussed on VP62, even Singh's latest, which only Silverman found. The WPI is not finding VP62 but a range of MLV related viruses which Lo also found. The two studies, minus Silverman's contribution, are virtually the same in outcome and much stronger in their findings. What Silverman's admission has done is bring the two studies closer together. None of the negative studies disproved WPI or Lo. Not one iota of evidence to support any argument that these other viruses are contaminants.

    In fact Silverman's admission has made all the negative studies irrelevant. To counter WPI's and Lo's findings, the anti HGRV crowd will have to start all over. The score should be restarted WPI + Lo (2); anti HGRV (0).
     
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  20. redo

    redo Senior Member

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    Having read more of your posts IVI which aren't writings between us, I have to take a strong reservation. Please do speak against XMRV, speak pro Wessely & Co, and disagree with me 100%.
     

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