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dr. Mikovits statement at 1st Intl conf..... please educate me..

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by voner, Sep 9, 2010.

  1. voner

    voner Senior Member

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    An excerpt from the Q&A session Webinar at the 1st international XMRV Conference:

    Dr. Mikovits "Were talking about DNA hypermethylation of these viral genomes in cells so that theyre not expressed. "

    Would somebody be so kind to explain the details of what she is saying here? That's a pretty definite statement she is making

    Thanks a million.

    Voner
     
  2. Daffodil

    Daffodil Senior Member

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    this is from a researcher:


    Sue,
    Well, this is one of the mechanisms we think is used in cells to keep integrated proviruses silent, and thereby contributing to the reservoirs of virus. Various cell types (embryonic stem cells, and hematopoietic stem cells, and likely others) can methylate the DNA of the proviruses, which keeps them silent. Presumably the benefit is to keep virus from replicating, but the downside for us is that it keeps virus present as silent DNA.
    How this plays out for a virus like XMRV is not yet clear.
     
  3. richvank

    richvank Senior Member

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    This is an issue that I'm very interested in. I would like very much to know how the partial methylation cycle block and glutathione depletion that we see in most PWME/PWC's meshes with the presence of the retroviruses. One possibility is that the proviruses are there, integrated into the person's own DNA before they become ill, but they are not expressed because the person has a healthy methylation cycle, and the proviral DNA is methylated, and therefore silent. Under this scenario, something else (any of a variety of physical, chemical, biological or psychological/emotional stressors or some combination of them) could deplete glutathione and bring on a partial methylation cycle block. This could potentially cause demethylation of the provirus DNA, resulting in expression of the retrovirus. This expression could cause other mischief in the pathogenesis of ME/CFS, perhaps contributing to its chronicity. I'm not saying that this is what happens, but I think it is a possible hypothesis at this stage of our understanding.

    Rich
     

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