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Proposition to put the XMRV discussion here on a more profound and scientific basis

Discussion in 'XMRV Research and Replication Studies' started by Waverunner, Jun 6, 2011.

  1. Enid

    Enid Senior Member

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    IVI - there is basically only one (for those who have been through the lot) criteria - the Canadian Consensus and any other is part only understanding and a compromise by so much exclusion.
  2. Bob

    Bob

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    Waverunner, for clarity, I'd like to point out that every single point that I've made in my lists, I can back up with evidence (e.g. published papers) or with statements/quotes/letters from virologists, such as from Alter or Mikovits. So my part of the discussion is science-based.

    Anyone please feel free to ask, and I'll be happy to provide links for any information that I've stated in this thread.
    The only thing that I can't yet back up with professional analysis, is the nature of the genetic variability of the WPI's new genbank sequences. But like I've pointed out before, genetic variability is not essential to potentially disprove the current contamination theories anyway (links can be provided to back this up).

    The only important thing for me is that the research into MLV-related viruses should continue.
    I'm not saying that there is an XMRV/CFS connection. I'm just saying that there is evidence to suggest that there might be, and the research should continue in order to determine the facts.
    But some people are saying that there definitely is not an XMRV/CFS association, but they are not basing their opinions on conclusive evidence. To not have conclusive evidence and to not want the research to continue, totally baffles me.

    It isn't important to me who is right or wrong in this debate, in the long-run.
    The only reason why I am involved in this discussion and pointing out the weaknesses of the contamination theories, is that I wish people to understand that the subject is not black and white, but is extremely complex, and that contamination has not been proven.

    I am an ME patient, and I wish for every avenue of scientific research to be explored.
    If the XMRV/CFS connection is ever proved to be a 'myth', then I'll swiftly move on.

    In the mean time, I read all the fascinating abstracts that have recently been published as part of the retrovirus conference, and the intriguing new XMRV papers that get published every month, and I know that there is plenty more XMRV research to be carried out before we even begin to understand this/these virus/viruses.
  3. Jemal

    Jemal Senior Member

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    Good post Bob. Or at least I think so :D
    I share the same opinion. I think the game is still on, regarding XMRV/MLV's. It's a very complex subject and it seems many virologists are groping around in the dark... which is to be expected in a new avenue of research like this, I guess.
  4. Bob

    Bob

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    Here are some of Harvey Alter's strong opinions regarding contamination.
    This is not a very recent quote, but I haven't yet seen any indication that he has changed his opinions.


    Blood Products Advisory Committee Meeting

    December 14, 2010

    Transcript

    Dr Harvey Alters Closing Remark at the Conference

    Invest in ME Website

    http://www.investinme.org/InfoCentre Topics Dr Harvey Alter BPACM.htm

    Extract:

    "But I still want to counter by saying I think the current evidence for disease association is very strong, even though not universally confirmed. But it has been confirmed now in at least four studies, two of which were presented today, that either XMRV or a polytropic MLV is associated strongly with chronic fatigue syndrome. A point that I think was misrepresented today: In those labs who do find the agent, it is very reproducible. Judy has found the same patients to be positive by culture year after year. We have found a patient to come back after 15 years and still be positive. So this is not a single, isolated finding. It's confirmed by sequencing. It's reproducible over time."


    Please read the rest... It's interesting!
  5. Bob

    Bob

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    With regards to Singh's research, she has contradicted her own results/conclusions in separate published papers.

    In her prostate cancer study, she detected XMRV in 4% (or 6%?) of healthy controls.
    This confirmed and validated the WPI's research which detected XMRV in 3.7% of healthy controls.
    But in Singh's CFS study, she was unable to detect XMRV in the blood of healthy controls.

    So, either Singh's prostate cancer study results were wrong, or her CFS study results are wrong.
    Instead of querying her own results, and asking if she was indeed able to detect XMRV in the blood, she simply concluded that XMRV is not associated with CFS, based on one single negative study.

    Singh's study looks sophisticated and complex, but if she was not able to detect XMRV in the blood using her methodologies, then that is the only conclusion that she should draw from her results. (The WPI has listed the differences in their methodologies.)

    When ask about these discrepancies, she said that she didn't know why there was a difference:
    "Not entirely sure, but there were different assays (e.g. immunohistochemistry) and different sample types (blood vs prostate tissue)."
    http://www.cfscentral.com/2011/05/dr-ila-singh-we-are-now-convinced-that.html

    So she admits that the zero results maybe due to different methodologies.

    But now, despite this, she has remarkably come to exactly the same conclusions as Stoye and Coffin, as if they were all reading the same script:

    "I'd urge people to move on rather than to keep their hopes hanging on the link between XMRV and CFS," says Ila Singh
    http://news.sciencemag.org/scienceinsider/2011/05/more-bad-news-for-chronic-fatigue.html

    Singh says about finding XMRV in prostate cancer patients:
    "This increases the population at risk for XMRV infection from only those homozygous for the RNASEL variant, to all individuals. Our goal is to further understand pathogenesis by XMRV, to determine if this virus causes prostate cancer, and delineate possible mechanisms for oncogenesis. We will also carry out epidemiological studies to study the prevalence and tropism of this new and important virus."
    http://projectreporter.nih.gov/project_info_description.cfm?aid=7866444&icde=4780366

    So if XMRV is such a serious virus that deserves such close attention, then why dismiss the association with CFS based on flawed results?

    HIV research had a very similar pattern of unexpected research outcomes in the early years.
  6. Bob

    Bob

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    There's a repeating mantra aimed at ME patients: "Move along... there's nothing to see... "


    Meet the objective professionals:

    Coffin:
    So Coffin says: "...these results essentially close the door on XMRV as a cause of human disease."
    That's a new one... I thought that prostate cancer was still being investigated, as well as CFS, and breast cancer, and autism.
    Research will not be shut down based purely on Coffin's personal biases, hunches and opinions.
    Switzer of the CDC has already challenged Coffin's study with a new paper, which dismissed Coffin's recombination theory. (link available - please ask).
    Maybe Coffin doesn't read other scientists' research.


    Stoye:
    "He said the implication was that the samples were contaminated, however this had not been definitively proven".
    So it has not been proven that the WPI's results are due to contamination, but XMRV is definitely not linked to CFS, according to Stoye!? How scientific!

    At least it is helpful of Stoye to admit that contamination has not been proven.
  7. markmc20001

    markmc20001 Guest

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    sorry Willow. Don't here often enough to keep up with the posts on a daily basis.

    Just saying a tactic used by special interests is to employ every available researcher "for hire" to gain advantage. For instance, BP tried to hire every marine biologist during the time of the oil spill and have them sign some kind of contract. Once the scientist has signed a contract, BP could effectively control the opinion of the scientist, or at least prevent her from publishing any evidence contrary to what BP wanted the public and government officials to know.

    Given the way research on health is funded by mostly Big Pharma, medical research is funded by Big Pharma, government agencies have Big Pharma employees on the boards, Big Pharma funds advocacy organizations, Big Pharma has media relations departments, etc...

    IF Big Pharma had a different vision for how XMRV research should come out, compared to that of the WPI of Alter et al, it is possible for the consensus to appear heavily weighted against the WPI. Even if the concensus was not accurate or non-partisan.
  8. Mark

    Mark Acting CEO

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    There are so many misconceptions in the above post that I feel compelled to respond, and will actually have to work at it a bit to do so politely...

    Several things wrong with this sentence; I'll mention a few...

    Actually, 'we' are not generally happy to use high illness population numbers for PR purposes. The CAA have regularly been criticised by many well-informed patient advocates for falling into the trap of using higher figures for prevalence. Seductive as it is to go for the headline figures, those who emphasise the importance of stricter criteria almost always emphasise also that the numbers of people said to have "CFS" have been grossly inflated in a way that hides the "ME" population. And this game of Russian Dolls with the definitions is only getting worse: a recent UK paper (involving both White and Wessely, I think) claimed very high incidence of "chronic fatigue" - defined extremely loosely and obfuscated in such a way as to confuse "chronic fatigue" with "chronic fatigue syndrome" - so much so that it would suggest that up to 2.5m of the UK population are affected! It's as if the definition were being diluted at a rate of 10:1 every 20 years or so in order to deliberately hide any useful scientific findings.

    And when the definitions are broadened like that, it ought to cut both ways: if they really are saying there are 2.5m of us, then it wouldn't be hypocritical to say that the UK certainly ought to stump up more than 800k a year to research the condition if this really were the case...while at the same time highlighting that continually broadening the definition is hiding the disease defined by the stricter historical definitions.

    And it is in any case valid to say that (eg) an estimated 17 million people worldwide are affected by CFS, where "CFS" is a slave-name definition encompassing many people who are all impacted to their detriment by the approach taken to research criteria, while at the same time arguing that in order to study that population of chronically ill people a tight definition is required.

    And I really don't like the way the word 'hypocrisy' is edged into that sentence, as a veiled straw-man accusation against an undefined population, especially because I've seen no such hypocrisy myself, in this thread or elsewhere.

    But the biggest and most important misconception of all in that sentence, IMO, is the idea that this is a question of who is "worthy of illness research". It just isn't about that at all. In a situation where the sick population is ill-defined, and the research and diagnostic criteria vary and encompass overlapping sub-populations, it's surely obvious that one of the best ways to make progress - for everyone - is to study those most severely affected and whose illness is tightly defined. Bob recently led an excellent discussion seeking consensus over campaigning criteria, and we identified that the single most crucial issue, and the one on which almost everyone from all viewpoints was agreed, was the importance of using the CCC for research purposes. Personally, I would not now fit the CCC, and it's questionable whether I ever did, even when I was most ill. But the best prospect for me of making progress with the understanding my illness is study of CCC-defined ME/CFS. And besides, I also recognise that those most severely affected deserve a special focus, and that historically more tightly-defined ME and CCC CFS has a very strong case for being studied as a discrete disease entity. Apart from which, other populations fitting Reeves-like definitions may be studied also, and the study of the CCC population does not exclude the study of other more loosely-defined populations who are less severely ill.

    So it has nothing to do with who is "worthy of illness research" - it is a question of studying a well-defined population, the core of the condition, in order to learn something about it which may very well turn out to benefit many of the wider population defined by Reeves and Oxford etc.

    A council of despair that applies to just about any campaigning issue: how to get loads of different people to start behaving rationally? And the issue of cohort definition is so crucial, so fundamental - as Leonard Jason explained in setting the scene at the NIH State of the Knowledge workshop - that progress just can't be made without it. So if it's hard to convince people of that, nevertheless there is no option but to work hard at doing so. And if many of them ignore that call, then those with CCC CFS who are seeking the truth will continue to be right to ignore and disregard the research that fails to study the CCC population, and to criticise its selection criteria as being irrelevant to CCC studies, on the basis that it is research that is studying a different population.

    Gosh, if causation or disease processes actually were the focus of research in the UK, or by those studying the looser Oxford-like populations, then we would be in a very different world indeed. Wessely for one will not advocate research that focuses on causation since he has stated many times that he does not believe the cause of CFS, GWI, etc (seemingly anything he researches!) will ever be found. (And when he does so he fails to add "...certainly not if I have anything to do with it.", as I think would be accurate).

    Anyway, you seem to be saying here that it doesn't matter if you study a much broader population, that won't matter if you find something, even if it's only in 10% of those studied. And again, that's untrue, in multiple ways. Firstly because it's obvious that if you pile on another 10 haystacks it's going to make it that much harder to find the needle. Secondly because the reality of a great deal of the scientific process around ME/CFS is in purported replication studies that claim to fail to replicate a finding because the percentages found are so much lower - in a different population! It's a transparent flaw in logic that's apparent to anyone who makes a minimal effort to explore the issues around ME/CFS, and it's so basic and obvious that it's really a challenge to attribute the persistence with this flawed approach to mere stupidity.

    Again, there's so much wrong with this. First we have the counsel of despair once again: this campaign can not be won quickly and easily (and what campaign can be I wonder??) - so, crucial though it may be, we shouldn't bother with it. Next "research could be pursued..." (if only...how do we achieve even that much?!) "...accepting Fukada/NICE as good enough"" - NO: It can't and won't be accepted as being good enough because it is not good enough...and I don't know what "NICE" is in a research definition context, but my own view (it's controversial) is that Fukuda actually does have some value as a starting point in a clinical context, but as a research definition it's clearly inadequate.

    To highlight the logic in a different way: IF it were true that the Fukuda-defined population were a homogeneous superset of the CCC population, then it would still be the case that a study of the CCC population would have the best chance of providing results that help the Fukuda population. So there is simply no downside to studying the CCC population, even if you believe that it's too strict a definition of whatever the discrete condition of the Fukuda population may be.

    At last, though, you end with a couple of points on which we can agree - and I'm all for looking out for those and building on them.

    "while disputing Reeves and other ad hoc rewrites (PACE)"
    - I'm so glad you agree on that, at least - the PACE criteria being the current state-of-the-art in obfuscation, misdirection and confusion.

    "and encouraging subtyping where appropriate is a way forward"
    - This too I think is a useful point in some contexts, which I would put this way: If certain researchers insist obstinately on studying a loosely defined and almost certainly heterogeneous population, then the very least they can be expected to do is to collect and release data enabling the identification of subsets within that population - with sufficient cohort size of the subsets to permit statistical significance in the results. But as that last point highlights, this simply means that in order to obtain scientifically useful information from such broadly-defined cohorts, those cohorts have to be that much larger - several times larger than a tightly-defined cohort - and the extra subsetting data has to be collected, analysed, and made available in order for the study to be useful...all of which increases the cost dramatically, of course.


    Dr Jason will be publishing his crucial work on a refinement of the CCC criteria in about September of this year, I believe. From what I've seen, I expect that definition - or series of definitions - to be a quite brilliant and seminal work in the definition of ME/CFS. There are problems with the CCC - I don't think anybody claims it is perfect - but Jason's work will hopefully resolve those issues, and then we really will have a strong basis on which to argue for the adoption of that new diagnostic framework for research purposes. In any case, the majority of the informed ME/CFS population will, I'm sure, continue to call strongly for the use of the CCC in ME/CFS research (and subsequently its successor in Jason's definition, I hope)...and those who choose to study something else and continue to find nothing useful will continue to be disregarded and denigrated by well-informed patients and their advocates.
  9. Mark

    Mark Acting CEO

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    An unreferenced and completely untrue allegation of being "anti-science", apparently levelled at the online ME/CFS community in general. I find it quite offensive. I haven't encountered a single poster on the subject of XMRV who is anti-science. I try to avoid generalisations, but here I feel confident in saying that everyone I know with ME/CFS is desperate to see much more scientific research into their illness, supports science and the scientific method, and simply seeks scientific understanding of ME/CFS. It is not science itself, but specific scientists researching XMRV and ME/CFS who have been strongly criticised - sometimes unfairly and excessively, I agree, but often quite rightly.

    The allegation of partialism, it seems to me, is simply an allegation/insult that people on one side of the argument about XMRV have lost objectivity and are blinded by prejudice or their own assumptions and desires as to what they want to be true. Of course all humans, without exception, are subject to such partialism, and that allegation can equally well be levelled at the other side of the argument - and much more fairly, in my opinion. Indeed, strong evidence in support of that can easily be found: many "anti-XMRV" scientists and protagonists have made public statements clearly indicating their own assumptions and prejudices, including (in nearly all cases) the pre-existing firm belief that ME/CFS does not have an infectious or viral cause, and does not have a single cause (and notably this particular partialism illogically attacks a strawman theory since it is an association that has been suggested here, not necessarily a cause).

    And is it not the case that the scientific community in general is somewhat 'partial' in their approach to any suggestion that an infectious retrovirus may have been created in the lab, spread by vaccines, and caused devastating chronic illnesses to millions? I submit that scientists themselves are not without their own blind spots - such possibilities, though perfectly plausible, seem to be completely unthinkable to most authorities in this area, and cannot be advanced or explored openly without provoking extreme and aggressive reactions. Those reactions extend well beyond the anger expressed by some patients online: they include attempts to curtail the careers of anyone who steps out of line and explores such unthinkable possibilities.

    Opposition to specific scientists in the "anti-XMRV" camp should not be confused with being "anti-science". Scientists who state that they are "1000% sure" of conclusions that are not logically supported by their research, who publicly announce their expectation that they will fail to find something before looking for it and then rapidly announce that they didn't find it and that means that it isn't there, who state that something has been "proven to be contamination" and advance inconclusive, circumstantial evidence in support of that claim, who manipulate the media and appear to have total control over what is advanced to the public such that they still don't even know the controversy even existed, and who claim a clear consensus of "the scientific community" even while a conference of scores of leading researchers is gathering to discuss 20 new abstracts disputing that consensus....such behaviour by scientists deserves to be distrusted and vociferously opposed.

    It may be bad public relations for the online ME/CFS community to express their disgust and distrust of such behaviour - but it would be bad strategy to keep quiet, trust, and wait for the scientists to do their thing...and it's even worse public relations for scientists themselves, in representing the scientific community to the patient community, to have behaved in the way that several have. It's those people, and their bad science, who have done the scientific community a disservice, and so it's they, as much as anyone, who deserve the label 'anti-science'. It's scientists, science journalists, and pseudosceptics who have destroyed my personal faith in the trustworthiness of much of the scientific community in the last 2 years - not angry patients.
  10. Jemal

    Jemal Senior Member

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    Quoted for truth. At least, this has been my experience as well. The scientific community has lost a lot of my respect.

    I studied computer science, the mathematical kind of science. Everything operates by logic. It was a bit of a shock to see how other avenues of science work... some of the conclusions in papers I saw were not logical at all and the evidence was not always there.
  11. Bob

    Bob

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    Thank you for putting the record straight Mark.

    Only if someone does not understand science themselves could they accuse forum members of being anti-science.

    And we could compile a long list of CFS researchers who have never complained about the ME community. Ever.

    It's notable that the only scientists who seem to complain about us are the ones who persist in making sweeping statements about CFS/ME which are not based on solid evidence.
  12. Sasha

    Sasha Fine, thank you

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    Hi all - lots of people here wanting to get to the bottom of the XMRV question but I only see one person so far (hi jace!) with a signature advertising the huge funding opportunity for WPI in the Vivint contest, the big-money round of which started yesterday.

    Resolving the XMRV question can't be done if WPI runs out of research money. Please take a look at the thread about the Vivint contest here and please consider making a signature like mine to advertise the contest (instructions here).

    Hijack over! :D
  13. Bob

    Bob

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    I had forgotten about this, but in one of his recent studies, Switzer specifically says that the XMRV sequence variation that he has detected is "consistent with virus evolution during spread and persistence." Switzers's evidence and conclusions directly contradicts the conclusions that Coffin and his co-authors have come to in relation to there being no variety in any XMRV sequences. Switzer indicates there is evidence of virus evolution expected during normal human infection in the wild.

  14. joshualevy

    joshualevy

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    Bob, are you going to post the name of even one Virologist (not employed by WPI) that thinks that the WPI genbank DNA samples are not evidence of contamination? If there is scientific controversy, that's one thing. But if every Virologist (not employed by WPI) says one thing, and none say the other (unless they work for WPI, of course!) then there isn't any controversy at all. There are just a bunch of forum posters who don't like the answer.

    Has Switzer, Lipkin, Lo or Alter come out saying that those DNA samples show that it's real?

    Joshua (not Jay!) Levy
  15. Jemal

    Jemal Senior Member

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    As has been said before I think: it's not that we don't like the answer. We think (or at least I do) it's premature to stop researching XMRV/MLV's as a possible contributing factor to our disease, based on the evidence presented so far. I am sure most of us wouldn't really want a nasty retrovirus... that some of us think it's our best hope for a treatment says something about the way we have been treated so far I guess.

    None of them have, that I know off. Do they have to make statements about it though? I haven't seen them come out and say those DNA samples show it's contamination either. More important is that all of them are still involved with and doing research on XMRV/MLV's. Switzer has done several negative studies, but he is finding XMRV on some samples nowadays (controls I think?). Lipkin has stated he remains agnostic at the moment and Alter has made statements that he still believes in his study. All three of them are involved in the BWG and Lipkin study I think...
  16. Bob

    Bob

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    Joshua, if you are going to post on the forum, then please be courteous enough to read other people's posts, and to engage with other users in a meaningful way. I've already addressed the points that you've raised in this post, a number of times.

    You don't seem to have a grasp of the science, which is perfectly OK, but please don't accuse other forum members of being ignorant, or anti-science, or biased, when it is you who does not have a grasp of the science, and it is you who seems to need or want XMRV to be a contaminant, for whatever reason. I believe that most forum members are open minded about the science, but you clearly are not. If contamination of the WPI's research is ever proved, then I will accept that. If contamination of Alter's research is ever proved, then I will accept that as well. You have concluded that the WPI's research is due to contamination without any conclusive evidence, or even the balance of evidence in your favour. Your conclusions are without foundation.

    All I can do is attempt to explain the science to you, and to present you with the evidence, but if you refuse to engage or to try understand the science that is presented to you, then I can't do anything about that, but I would ask you that you stop insulting other forum members.

    As I've already said, I'm not aware of any researchers making any conclusions either way about the WPI's latest genback samples in a peer reviewed analysis.

    But as I've also explained, there are a number of reasons why a lack of variety in viral sequences does not prove contamination, and I have provided references to articles in scientific journals which demonstrate this. (5)

    I'm personally not aware of any scientists who have said that the WPI's newest sequences prove contamination. Are there any? You are wrong to say that no scientists, except those employed by the WPI, believe that the WPI's results are not due to contamination. I am aware of quite a number of scientists who believe that the WPI's research is not due to contamination... Please see below...

    If you are refering to one or two scientists expressing opinions about the WPI's most recently published XMRV sequences then that isn't evidence. There has been no peer reviewed analysis of the WPI's newest sequences.

    You insist that the WPI's findings are due to contamination, but you can't provide conclusive evidence for this.

    These are the contamination theories that we have to date:
    1. False PCR readings (i.e. cross reactivity).
    2. Mouse DNA contamination.
    3. XMRV is a mouse virus.
    4. DNA contamination from a cell line.
    5. XMRV is purely a cell line virus (Purely a lab artifact).
    6. XMRV is a wild human virus but doesn't exist in CFS patients.

    The WPI has been accused of all of these, and so it's difficult to know which one we are up to at the moment.

    There seems to be a general scientific consensus that the first 4 have now been disproved, so we are left with theories 5 and 6.

    Theory 5:
    The latest accusation, from Coffin & colleagues is that XMRV is a real virus, but that it only exists in cell lines, as a laboratory artifact, and it doesn't exist in the wild, and hasn't infected humans. So these scientists subscribe to theory 5.

    However, other prominent scientists do not subscribe to theory 5 because they have detected XMRV in human tissue (1) (3) (11)... So the weakness of theory 5, is the evidence provided by other scientists such as Singh and Switzer, which demonstrates human infection (1).

    So that explains one of the weaknesses of theory 5. But alongside this, the two recent Switzer studies demonstrate XMRV genetic variability (1) and also challenge Coffin's recombination theory (8) (9), thus opening up the possibility that XMRV originated in other places, other than the cell line that Coffin investigated. So this evidence demonstrates further weaknesses in Coffin's and his colleagues' conclusions.

    Theory 6:
    Singh's theory is slightly different to Coffin's because, when she is refering to her prostate cancer study (3), she believes that XMRV exists in the wild, in prostate cancer patients and in the normal healthy population at 4% (or 6%?). But when Singh is talking about her CFS study, where she tested blood instead of prostate tissue, she fails to detect XMRV, and concludes that XMRV doesn't exist in CFS patients or in the normal healthy population. The weakness of Singhs conclusions is that they are conflicting, based on different results using different methodologies. In her CFS study, XMRV exists in 0% of the population, but in her prostate cancer study, XMRV exists in 4% (or 6%?) of the normal population. So, Singh apparently subscribes to theory 6, although in a rather contradictory fashion, as her prostate cancer study suggests that at least 4% (or 6%?) of CFS/ME patients should test positive for XMRV. It seems to me that Singh has demonstrated only that she can detect XMRV in tissue, but not in blood samples. She has no other explanation for the discrepancies (4).

    Switzer also believes that XMRV is a real wild human virus (1), but that it doesn't exist in CFS patients, so he also subscribes to theory 6. However, his opinions are also contradictory, because he admits in a recent study (1) that he has inadequate methodologies to detect XMRV in the blood of any individuals, even when he has confirmed them to be XMRV-positive by testing those individuals' prostate cancer tissue.

    So the weakness of theory 6 is the fact that the scientists who have published some of the zero/zero XMRV studies, looking at the blood of CFS patients, have demonstrated that they are unable to detect XMRV in the blood of XMRV-positive patients. This gives us a good reason to suspect that it might be the methodologies that are at issue, rather than an absence of XMRV. There might be other reasons for the discrepancies, but we just don't know the exact reasons at the moment, and nor do the scientists.

    The other weakness of theory 6 is the consistent results from the WPI, and the strength of all of their various findings. Then there are the related MLV sequences that Alter and Lo detected. These findings suggest that further research into human infection from MLV-related viruses is worth continuing with.


    In terms of the specific allegation that the WPIs results are purely due to contamination, this has been argued over endlessly, so I will just repeat the following... As I have explained earlier, a lack of sequence variability is not proof of contamination for the following reasons:
    1. XMRV Mutation behaviour could be similar to HTLV. (6)
    2. There could be alternative routes of XMRV transmission in humans such as in vaccines. (5)
    3. The WPI have many more XMRV isolates that they have been unable to sequence and publish due to a lack of funding. As our knowledge about XMRV, and the evidence relating to XMRV, continues to grow, then a higher variation in genetic sequences might become evident.
    4. A variety of MLV-related sequences such as P-MRVs have been detected by various researchers including the WPI. (10)
    5. The consistent nature of the WPI's results, and the strength of their original Science paper suggest that they haven't detected contamination.


    So are you saying that XMRV is a contaminant only in the WPIs research, or are you saying that XMRV is not a real or wild human virus? These are two entirely separate issues.

    As a direct answer to your question, here are the virologists that spring to mind who believe that XMRV is a real virus... And I'm sure that there are more:
    Switzer (1), Alter (7), Russceti, Beiger, Hanson (12), Silverman (2)

    Alter strongly believes that the WPI's research is evidence of a real human virus in CFS patients (7) (Quotes given earlier in the thread.)

    Switzer has provided his own XMRV sequences to genbank (1) which he concludes is evidence that XMRV is a real, wild, human virus, due to the genetic variability.


    References:

    (1) http://www.plosone.org/article/info:doi/10.1371/journal.pone.0019065#abstract0
    No Association of Xenotropic Murine Leukemia Virus-Related Viruses with Prostate Cancer
    Switzer.
    "Sequence analysis of the PCR-positive specimens was highly informative because it confirmed that all three specimens were XMRV-related. Also, the finding of a viral strain in three prostate cancer patients that is distinct from the XMRV seen in previous studies is significant and demonstrates a broader viral diversity. This would be an expected result consistent with virus evolution during spread and persistence."

    (2) http://www.retrovirology.com/content/pdf/1742-4690-8-S1-A241.pdf
    Human infection or lab artifact: will the real XMRV please stand up?
    Silverman.

    (3) http://www.pnas.org/content/106/38/16351.full
    XMRV is present in malignant prostatic epithelium and is associated with prostate cancer, especially high-grade tumors
    Singh.

    (4) http://www.cfscentral.com/2011/05/dr-ila-singh-we-are-now-convinced-that.html
    Interview with DR. ILA SINGH
    "Not entirely sure, but there were different assays (e.g. immunohistochemistry) and different sample types (blood vs prostate tissue)."

    (5) http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(11)70081-0/fulltext
    Mouse viruses and human disease
    Gkikas Magiorkinis.

    (6) http://forums.phoenixrising.me/show...it-can-explain-XMRV-s-low-degree-of-mutations
    HTLV-1's replication: Perhaps it can explain XMRV's low degree of mutations

    (7) http://www.investinme.org/InfoCentre Topics Dr Harvey Alter BPACM.htm
    Blood Products Advisory Committee Meeting Transcript
    Dr Harvey Alters Closing Remark at the Conference

    (8) http://retroconference.org/AbstractSearch/Default.aspx?Conf=20&Abs=40126
    Extensive Genetic Recombination in the XMRV Genome
    Switzer.

    (9) http://www.retrovirology.com/content/8/S1/A235
    Murine leukemia viruses (MuLV) and Xenotropic MuLV-related viruses exhibit inter-tropic complex recombination patterns
    Switzer.

    (10) http://www.pnas.org/content/early/2010/08/16/1006901107.full.pdf html
    Detection of MLV-related virus gene sequences in
    blood of patients with chronic fatigue syndrome
    and healthy blood donors

    Alter & Lo.

    (11) http://www.retrovirology.com/content/8/S1/A222
    Prevalence of XMRV in blood donors, HTLV and HIV cohorts
    Abbott Diagnostics.

    (12) http://www.retrovirology.com/content/pdf/1742-4690-8-S1-A234.pdf
    Detection of MLV-like gag sequences in blood samples from a New York state CFS cohort
    Hanson.
  17. Bob

    Bob

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    Extracts from Amy Dockser Marcus' latest Wall Street Journal Health Blog:

  18. Bob

    Bob

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  19. markmc20001

    markmc20001 Guest

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    Hey Bob,

    Your a superstar. Thanks for all your hard work. With all the time you have invested, I hope you can consolidate all your evidence into one paper or even write a book. Might be useful in getting the complete story out considering various media outlets don't cover the story as you lay it out. Could also be invaluable for raising private funds for more research.

    My impression is the CFS patient population/researchers taking interest and time to read here probably consider themselves above average intelligence. Most everybody who has followed for a few months can get the general idea things are not complete and there are still many flaws with the logic as you point out. Even though I can't understand the science as well as many here can, I would like to mention I can easily cross reference your links and get the facts.

    Thanks again to your clear and concise posts.
  20. madietodd

    madietodd Senior Member

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    There are people in PR who have tested positive for XMRV. I don't see how that would be possible if XMRV didn't exist in human populations.

    Madie

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