New Atmosphere, New Vision: Gibson and Whittemore Kick Off Invest in ME Conference 2016
Mark Berry reports on Dr. Gibson's introduction and Dr. Whittemore's keynote speech, at the 11th Invest in ME International ME Conference in London.
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New Nature Paper on XMRV

Discussion in 'XMRV Research and Replication Studies' started by RustyJ, Jul 20, 2010.

  1. RustyJ

    RustyJ Contaminated Cell Line 'RustyJ'

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  2. garcia

    garcia Aristocrat Extraordinaire

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    Yes it is new. Thanks for the link!
     
  3. taniaaust1

    taniaaust1

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    Its just a review on what is known so far.. Silverman is one of the ones who already have done a study on it
    (I'd gotten all excited, thinking it was a new study till i looked).

    Thanks for sharing .. any unbias publicity I think is good :)
     
  4. Marco

    Marco Grrrrrrr!

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    I strongly object to being called a 40 to 50 year old woman!:Retro mad:
     
  5. RustyJ

    RustyJ Contaminated Cell Line 'RustyJ'

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    Why do they even bother to say things like that? These are scientists, supposedly with some contact with patients. Surely they would have some sensitivity and not add to stereotyping. There is not even a reference for this statement. Very unscientific, unprofessional, lowers the tone of the paper. As far as I am concerned there has been very little research done on ME patient gender. Hardly anyone has bothered. (Oh, btw I am also not a 40-50 year old woman, and I am ranting)
     
  6. CBS

    CBS Senior Member

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  7. RustyJ

    RustyJ Contaminated Cell Line 'RustyJ'

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    This paper seems to emphasise the point that there is almost no difference between the prostate cancer strain of XMRV and the ME strain, which seems at odds with other reports I have read. I am also wondering if they are working along the lines of XMRV causes ME mostly in women and prostate cancer (mostly) in men, although it would be odd for women to get prostate cancer.
     
  8. Ash

    Ash aka @smashman42 'SortaDerpy' on Twitter

    Here I was thinking I was a 31yo man.... :tear:
     
  9. taniaaust1

    taniaaust1

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    Silverman... is a cancer expert.. not a CFS expert. I assume the ones who did the review with him are probably buddies of his in same field. Hence what they know about CFS is probably not much more than the average person knows (certainly not what a CFS expert knows).. and it has been commonly said that most CFS people are in the 40-50 year age bracket so not knowing any better, they are making statement on what they believe they do know. (That age figure probably came out of the CDC!!! .. with their stupid CFS fatigue definations.. so we probably cant blame the ones who did this study on not knowing any better ).
     
  10. taniaaust1

    taniaaust1

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    yep.. correct thought.. any stupid CFS stuff always comes from the CDC. They must of included LOTS of elderly people in their so called CFS (ideopathic fatigue) defination and that put the average age up.

    from http://www.cdc.gov/cfs/cfsbasicfacts.htm#prevalence
     
  11. V99

    V99

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    Yep, had this 17 years, and still not reached my mid 30's.
     
  12. caledonia

    caledonia

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    If they are suggesting this, it's incorrect information. There are 3 strains of XMRV found in prostate cancer, and 6 other strains found in CFS.

    CFS XMRV strains = WPI-1130, WPI-1138, WPI-1169, WPI-1104, WPI-1106 and WPI-1178
    prostate cancer XMRV strains = VP35, VP42 and VP62

    ps. I love it that the CFS strains are named after the WPI.
     
  13. Eric Johnson from I&I

    Eric Johnson from I&I Senior Member

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    Actually those authors are right about this. VP62 and WPI-1104 are major bro's. They grew up together, at least early on. Their filial tenderness I will not even attempt to put in words. One was lovingly adopted by the WPI and the other by Cleveland/whoever - hence the disparate names which tend to confuse. VP__ and WPI-___ are not clusters of genetic relatedness, just names given to samples probably at the very moment of sampling.

    This moving tale is told in the Lombardi et al supplement. I don't know much about viruses - I don't know if these ones recombine, so I'm not sure whether you can really make a perfect tree of descent (phylogeny). The tree may also use assumptions of parsimony and thus be a little probabilistic... but I assume it's "generally meaningful" or one would (probably!) not make it. Anyway while VP62 (prostate cancer) and WPI-1104 (CFS) are one another's nearest siblings, every last one of them is very very close.

    Odds are pretty high, I would think, that most or even all of the nucleotide differences have no significance for the function of the virus, or have a nonzero but totally negligible functional significance. That's certainly how it is in most organisms, actually all organisms I know of.

    Of course, humans recombine and you can still make family phylogenetic trees for us. But they will not be cleanly ramifying like the trees of an organism with no genetic recombination (sexual reproduction), as the one in Lombardi et al is - like an actual tree, a real physical tree growing out of the ground. Instead of that, they will be hugely tangled like lace, because each descendant has more than one parent.
     
  14. anciendaze

    anciendaze Senior Member

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    I will generally agree with Eric Johnson on this. The nucleotide differences I have seen are useful for distinguishing possible laboratory contaminants, which these do not appear to be, but they do not affect the sequence of amino acids derived from those genes. If this were a familiar virus, they would all be classified as the same thing.

    The subject of recombination has come up repeatedly recently. If the kinds of recombination several have suggested are taking place, the resulting sequences would be dramatically different. This could affect the ability of nested PCR to find sequences. There is considerable uncertainty about where and how this might occur. I'm betting on recombination of RNA sequences from several viruses infecting the same cell, not DNA. This parallels some natural processes used by the immune system to generate huge numbers of antibodies with a modest number of genes.
     
  15. gracenote

    gracenote All shall be well . . .

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    The paper says that possible "reasons for differences in the detection of XMRV in both prostate cancer and CFS" in the different studies "could include the following":

    1. Contamination: "Contamination cannot, however, account for all positive findings of XMRV in humans, which are based on multiple lines of evidence from different laboratories . . . Furthermore, the nucleotide sequences of XMRV are similar but not identical to any known strain of MLV, which limits the likelihood of contamination from mouse sources."

    2. Geographical Differences: "Geographical differences in the distribution of XMRV are likely to account for some, but not all, of the differences in findings."

    3. Sequence Variation: "Sequence variations in XMRV, or XMRV-like viruses, could explain why some studies fail to detect XMRV. While XMRV strains that have been reported to date are more than 99% identical, the existence of divergent or related viruses is possible and these could easily be missed by many of the methods, in particular PCR, used to search for XMRV."

    4. Clinical Criteria: "In CFS studies, clinical criteria for patient selection varied (Oxford, CDC or Canadian criteria) between the different studies, which might have contributed to the different findings of XMRV."

    5. Absence of Standardized Detection Methods and Positive Control Samples: "The absence of standardized, highly sensitive methods of detection coupled with a lack of widely available, positive control human samples is likely to contribute to the different results obtained between studies."

    [Nothing new, but nice to see it spelled out, just the same. Could add this "reason" to the CFS studies: 6. Determination to NOT find XMRV.]
     
  16. RustyJ

    RustyJ Contaminated Cell Line 'RustyJ'

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    Spurious logic. Assumes ME patients recover or that condition is for a limited period. Given equal distribution across all ages for initial infection, then its stands to reason less children would have it than adults. Also people in their 40s and 50s more likely to have had the condition for a longer period of time, hence greater chance of being labelled ME or CFS. Patients with short-term illness or of younger age more likely to be labelled as some other condition at least for a while.

    There simply is no reason yet to assume different ages or sexes are more likely to contact XMRV. Also completely ignore the fact that the virus can lie dormant for decades.

    Also it seems the Nature review has combined two seemingly unrelated facts: one that 4 times women to men are likely to have ME, and two, people in their 40s and 50s more likely to have ME. I know it's nitpicking, but you can't really combine the two facts.

    Still annoyed about the fact that respected researchers have chosen to perpetuate flawed facts.
     
  17. Eric Johnson from I&I

    Eric Johnson from I&I Senior Member

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    According to a paper with Prof. Jason as an author, the prevalence isn't much lower in adolescents aged 13-17 than it is in adults - they found 0.18%. They acknowledged that this was a good deal higher than the numbers that previous work had found. I haven't read any of the papers but I think highly of Jason.

    Abstract doesn't even name the case def used, but with Jason's being involved I'm sure it was a legit def.

    Prevalence in pre-adolescent children was lower.
     
  18. SOC

    SOC

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    I'm guessing some teens with ME/CFS get labelled with "it's just being a teenager" and their symptoms ignored until they're really sick or are trying to work full time. I don't think anyone would have caught my teen's symptoms if we weren't already well aware of the symptoms through my experience.
     

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