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Dr. de Meirleir's poster at the XMRV Workshop

Discussion in 'XMRV Research and Replication Studies' started by richvank, Sep 10, 2010.

  1. mojoey

    mojoey Senior Member

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    Hey acer2000,

    So far, aren't the percentages of healthy people testing pos (4-7%) somewhat similar to the percentage of HIV+ that don't eventually get AIDS (10% based on what you just said). And we haven't had enough time to see if those healthy people who tested XMRV+ pos may eventually get sick.

    HIV works by crippling the immune system. Gammaretroviruses may work by doing the same, just not as fast.

    Eventually we would need long-term studies to show the difference in percentages between HIV+ people getting AIDS and XMRV+ people getting ME/CFS) are statistically significant.
  2. acer2000

    acer2000 Senior Member

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    Its actually less than 1% of people who carry HIV that don't get AIDS and die within 10 years. (I just looked it up). So basically everyone who carries HIV eventually dies of AIDS.

    According to a source cited in Wikipedia:

    http://en.wikipedia.org/wiki/Long-term_nonprogressors

    Just some numbers pulled out of a hat for example. If 5% of the total population carry XMRV (that would be 15 million in the USA), but only 10% of that xmrv carrying population (1.5 million of that 15 million) get ME/CFS, then the percentages are much reversed from HIV/AIDS. That would mean 90% of XMRV carriers *don't* get sick.

    According to the article on wikipedia on HTLV, between 1/20 and 1/25 people who carry it eventually develop the cancer or other illness associated with it. A much lower, but not insignificant, disease rate when compared to HIV.

    http://en.wikipedia.org/wiki/Human_T-lymphotropic_virus

    But its impossible to make this comparison at this point because A) we don't know what illnesses XMRV causes (if any) and B) we don't know the latency of XMRV. Its much harder to figure out the epidemiology of an infection if it takes decades for it to cause illness because on the surface all you have is how many people have the illness at any given time and an estimation of the carrier rate. It will take a lot of long term observation of the population to figure out how many of those carriers convert to illness and in what time frame. Perhaps they can do some retrospective studies on people who either developed CFS, prostate cancer, or lymphoma. That might give a head start.

    The other thing is... do we even know if the studies done on healthy controls for XMRV are large enough or designed in the right way to properly predict the virus prevalence in the general population? How many people need to be in a study to accurately do this? Any statisticians out there? Are the 3-7% results from these studies likely to be representative of the real population?

    acer2000
  3. MDL

    MDL

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    Hi Joey,
    This assumes that HMRV/XMRV is to CFS/ME what HIV:AIDS. I don't assume that. It is also important to point out that XMRV is not HIV or AIDS.
    Rather, by my logic it would be:
    Gram-negative (or H2S+) is to HMRV/XMRV what gram-negative (or H2S+) is to HIV. These are theorems, not proofs.
    Further, without wading into a minefield, is is widely agreed upon that HIV causes AIDS, but technically, prevailing wisdom isn't absolute proof, even when we would wish it to be so. I do believe that an opportunistic virus favors the unprepared host.
  4. natasa778

    natasa778 Senior Member

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    London UK

    I think those are VERY rough estimates and may not be accurate at all...

    some food for thought here: http://www.washingtonpost.com/wp-dyn/content/article/2009/03/14/AR2009031402176.html

    "...the report also cautions that "we know that the true number of residents currently infected and living with HIV is certainly higher..."
  5. pictureofhealth

    pictureofhealth XMRV - L'Agent du Jour

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    Ah, so we're back to the 'germ theory of contamination' v 'the terrain is everything' (tie), once again. Unfortunately for us, I don't think the 'tie' proposal gets much government funding, as there are too many diverse possibilities.

    If XMRV, and/or related MLV's, aren't proven to 'directly cause' ME/CFS in the short term, then I don't think the big funders are going to stick around to do longitudinal studies on 'healthy' XMRV controls to look for other adverse outcomes such as cancer, neuro disease - again, too many diverse possibilites.

    The good news is that the WPI and other ME/CFS specialist physicians (in the US anyway) are patient focused, so at least some patients will continue to get some treatment to improve the immune system functioning (and host terrain), although this is way too expensive for the vast majority of us.

    Hopefully in the longterm the WPI's and others' research will prevail, consistent immune markers will be found and perhaps at the very least we can have more Ampligen trials and anti viral treatments (in the UK we are denied even that).
  6. alex3619

    alex3619 Senior Member

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    Hi Hope123,

    XMRV loves macrophages: there are lots of those in the gut wall, it is part of the immune defence. If these macrophages are infected with XMRV, then the gut wall is an XMRV reservoir.

    Bye
    Alex

  7. Cloud

    Cloud Guest

    I think this is quite possible.
  8. Daffodil

    Daffodil Senior Member

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    may i ask where you heard that XMRV loves macrophages? i thought gammaretroviruses usually only infect dividing cells?
  9. lansbergen

    lansbergen Senior Member

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    http://hvd.ens-lyon.fr/human_virolo...ases-of-the-retroviral-life-cycle-a-cimarelli


    Simple retroviruses cannot infect non-dividing cells (the importance of the exception)
    Although it is commonly accepted that simple retroviruses such as murine leukemia viruses (MLV) are impaired in the infection of non-dividing cells, as they have not evolved -contrarily to lentiviruses- to bypass an intact nuclear membrane barrier, we have recently found that primary human macrophages are the exception in which, despite the absence of cell division, MLV infection occurs rather efficiently. This exception to the rule suggests that something other than -or in addition to- the nuclear membrane barrier influences MLVs ability to infect non-dividing cells more generally. We are now trying to identify the factors that are responsible for successful infection of macrophages by MLV.

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