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The best studies on viral involvement in ME/CFS? EBV, HHV6-7, CMV etc

Discussion in 'General ME/CFS News' started by olliec, Sep 24, 2011.

  1. olliec


    London, UK
    A UK TV doc (Christian Jesson) has told me there is no evidence of viral involvement in ME/CFS, and I was wondering if anyone would be kind enough to let me have links to papers that do show involvement (I'm not looking for proof of causation)?

    I've sent him the ICCME but I'm consistently amazed by how little interest many doctors seem to have. Although happy to say yesterday I chatted with a trainee doctor who was very interested in the current state of research, and eagerly accepted a copy of the ICCME.
  2. heapsreal

    heapsreal iherb 10% discount code OPA989,

    australia (brisbane)
  3. Esther12

    Esther12 Senior Member

    This one finds that the severity of initial infection for three different types of infection is the best predictor for the development of CFS.

    It's not about on-going infection though.
  4. In Vitro Infidelium

    In Vitro Infidelium Guest

    It rather depends upon what definition of 'involvement' you are using- for instance do you include 'predisposition' as 'involvement', if that were the case then there is likely some epidemiological evidence (prior EBV infection etc) however if by 'involvement' you mean evidence of virus specific disease processes then there is no definitive evidence across the wider affected population. There is a difficulty with investigating viral role in M.E/CFS because tests need to be virus specific and there is a test of prior plausability to be met - to date there is no known infective agency that differentially affects human males and females, other than is mediated by physiological differences (no infection if you don't have the tissues which are prone to infection) or gender specific exposure) - this is a problem in M.E/CFS where a female/male prevalence differential is consistently reported. This means that not only does the question whether multiple infective agencies are implicated (both across the affected population and in individuals) have to explored, but there also the requirement for evidence to support a novel gender differential of infectivity.

    Of course the reported gender differential may be an artifact of diagnostic bias - there seems to be an absence of male manual workers from the reported demographics which could indicate a bias, either a result of diagnostician bias (M.E/CFS is psychological/a woman's disease) or some conflationary/masking effect where males are more likely to be diagnosed with occupational or lifestyle disease in preference to M.E/CFS. However at present the evidence is for a strong gender differential, and without an explantion for that differential, infective agency, partcularly a single infective agency across the affected population will be open to significant question.


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