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Hunting down the cause of ME/CFS & other challenging disorders - Lipkin in London
In a talk to patients in London on 3rd September, Dr. W. Ian Lipkin described the extraordinary lengths he and his team are prepared to go to in order to track down the source of an illness, with examples ranging from autism to the strange case of Kawasaki disease.
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HTLV-1 / XMRV Conference starts today!

Discussion in 'Media, Interviews, Blogs, Talks, Events about XMRV' started by VillageLife, Jun 4, 2011.

  1. currer

    currer Senior Member

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    Exciting, isnt it?.....I'm going to have a rest, now.

     
  2. Bob

    Bob

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    It looks like Switzer is challenging Coffin's opinion that this specific recombination event can only be one in a trillion.
    I think he is saying that it is far more likely.
    This is based on looking at a number of MLV genomes, taken from genbank, and seeing if they could recombine into a short XMRV sequence.
    He says that it is very likely, and that's only based on a small sample of MLV genomes that he studied.
    It blows Coffin's conclusions out of the water!
     
  3. Bob

    Bob

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    Yes, my head is hurting too!!! :cool:
     
  4. Bob

    Bob

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    Yes, I totally agree with you there currer.
     
  5. Enid

    Enid Senior Member

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    Thanks all for the information - looking very exciting.
     
  6. Jemal

    Jemal Senior Member

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    Bieger is a different study? So I don't understand your reply :D
     
  7. Bob

    Bob

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    Ah, yes, sorry!!!

    I'm easily confused!!!

    :confused: :confused: :confused: :confused:

    Please ignore that post... I'll go back and delete it!

    Hope i didn't confuse you too much Jemal! (Well spotted by the way!)



    (I don't have any idea why De Meirlier might have withdrawn his paper.)
     
  8. Jemal

    Jemal Senior Member

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    DeMeirleir should be speaking on the symposium "XMRV, a recently discovered human retrovirus: What do we know about it?" being held on 9 june.
    Patients are also going, so we should get some reports.
     
  9. alex3619

    alex3619 Senior Member

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    Contamination revisited.

    I am still thinking about recombination arguments. There are several points.

    Let me state again, before I begin, that Coffin's result could have been from contamination from infected lab workers or mice. Were they tested? Some others are also asking this question, but I leave it to them to speak.

    The argument that recombination derived XMRV is highly improbable is based on flawed probability calculations. I wish an expert on probability would get with a retrovirologist, and really look at this. It is unlikely that recombination is totally random. Highly unlikely, although I could be wrong. That alone makes the math suspect. So the real probability is not likely to be so remote. In addition, once you factor in all the species, all the MLVs, and all the recombinations, XMRV might have arisen in many different vectors. A particular strain of mouse using in prostate cancer culture creation is only one candidate.

    It is highly improbable that the cell line in discussion is the only place it could have happened. Therefore, purely on the basis of probability, but presuming other MLV recombinations could give rise to XMRV, it is highly improbable that it arose in the cell line. The argument rests on XMRV suddenly appearing in the cell line. I ask again: have they ruled out contamination?

    Please do not misunderstand the power of evolution. I spent some time studying the math behind genetic algorithms. Simple mutation is a minor and not very powerful mechanism for change. The real power in evolution is recombination.

    The following calculation is only indicative, based on rough guesstimates, which make it highly unscientific. I am just trying to get a sense of things. I would like to see it done by someone with real expertise in this area.

    Lets look at the total mammalian population in the world. It has to be many many billions - maybe hundreds of billions (many trillions?). If only 0.1% are infected with MLVs, then the total number infected is hundreds of millions. But wait, these individuals have numerous viral replications, in probably millions of cells. Lets be a little conservative, although the exact number is not very relevant. Lets say there are only a billion in the life of an individual. That is maybe one hundred million billion potential recombination events. Let me be sure we are on the same page, I mean 100,000,000,000,000,000 events. This could have happened over a century - call it ten generations, although this is also conservative. So we have ten to the eighteen possibilities. What are the odds that XMRV did not arise in one of them? Given that it might not be entirely random, and so simple probability math may not be valid?

    It is worse than this. This ignores the multiple sequences of recombination events. It is much more likely, based on my admittedly limited understanding which could be wrong, that XMRV arose several times.

    The only way to argue against this is to say that recombination events are rare - and that does not seem likely. Once it arose, it can spread and further mutate. How many mammalian species have been tested for XMRV infection? Does this include cats, dogs, cattle, sheep, bats and wild rats? How about all the other mammals?

    There are still huge questions about XMRV and MLVs in humans. All I am saying is that contamination by a lab derived XMRV strain is not the only possibility. Please note that any of the numbers I used in my calculation could be wrong - please feel free to substitute your own.

    The abstract by Prosperi, Switzer et. al. indicates that recombination is common, and it could result in XMRV.

    I hope the Hanson study is a precursor to the BWG and Lipkin, although I also dread it being right. I don't want a "new" retrovirus rampaging through the world populations - but if one is the sooner we find out the better. Bring on the research!

    The pressing question question to me is how did Erlwein et. al. get contamination but not in controls? Does anyone know the details? They claim to have something to say about the source of contamination. Depending on what it is, it could be important.

    Bye
    Alex
     
  10. Jemal

    Jemal Senior Member

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    Thanks Alex, a lot of text, but I could follow it easily. I am with you here that recombination events might not be that rare.
    Mammals also have a low life expectancy and they breed a lot, creating a lot of oppertunity for a recombination event I think. Also they are everywhere where humans are.
     
  11. Bob

    Bob

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    Hi Jemal,
    Would you mind doing me a big favour please?
    Could you add the latest abstracts from your recent post (link) to your original list of abstracts (link) please?
    This is so I can create a link to your post, with all the info in it, as a handy reference.
    Hope that's not too much bother?

    Or if you unable to do it, then I can copy and paste the info into a new post.

    Thank you,
    Bob
    :thumbsup:
     
  12. Jemal

    Jemal Senior Member

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    It's done Bob, I edited my original post.
    I am hoping for more abstracts by the way, the last 4 were just articles and not PDF downloads.
     
  13. Bob

    Bob

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    Thanks very much Jemal. Much appreciated. :thumbsup:
     
  14. eric_s

    eric_s Senior Member

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    I agree this will be interesting. But what sort of controls were these? It sounded a bit like it was not samples of the same kind as the cases.
     
  15. Bob

    Bob

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    I saw McClure's name associated with that paper, and decided not to pay too much attention to it!
     
  16. Jemal

    Jemal Senior Member

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    LOL

    (had to post a few more words, because otherwise the message was too short)
     
  17. Bob

    Bob

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    Regarding the theory of recombination in a prostate cancer cell line, I read a new possible theoretical scenario recently.
    It might be the case that the XMRV in the prostate cancer cell line actually originated in the human prostate cancer sample, and not in the mouse/mice.
    But Coffin et al. were unable to detect the XMRV in the original prostate cancer sample, or the earliest cell line, due to low copy numbers.
    It might be the case that the cell line is a perfect breeding place for XMRV to replicate, and so after the cell line had been propagated for a while, XMRV copy numbers increased, which enabled detection.
    So their whole paper might be based on a false theory, due to inadequate detection techniques.

    I can't remember where I read this... If I find the quote, I'll add it to this post.
     
  18. WillowJ

    WillowJ Senior Member

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    nice, thanks :)
     
  19. WillowJ

    WillowJ Senior Member

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    That's true that it's highly unlikely that recombination is random, but this is genetics, not probability. Shouldn't Coffin know this?
     
  20. omerbasket

    omerbasket Senior Member

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    I think that the following study seems like a very important one:
    http://www.retrovirology.com/content/8/S1/A235
    I have to say that I find it very hard to understand some of the things written there, but I'll try to do it anyway and please correct me if I'm wrong. Coffin's paper says the following:
    His probability calculations seem arbitrary to me, prboably not taking into consideration the charachetristics of MLVs.

    Anyway, look at the things that the paper written by Prosperi, Switzer et al. says:
    First of all, I'll continue a little bit with Coffin's paper. It says:
    But Switzer's abstract says:
    So, if XMRV is a recombinant of ecotropic MLVs with the two other types - why does Coffin's Pre-XMRV1 and Pre-XMRV2 are just xenotropic or polytropic/modified polytropic? By the way, that's still a question, so again - I'm open to hear why I might be wrong.

    Secondly, as I quoted above, Coffin says that the probability that an identical recombinant was generated independently is almost impossible. I don't know if he mean and identical recombinant meaning that his "pre-XMRV1" and "pre-XMRV2" would have met each other somewhere else, or that he means that another even would create XMRV, but in both cases, it seems to me the the following sentences seems to go directly against his argument (that it must be that XMRV was created without human intention only once, and it was with the pre-22Rv1 cell lines):
     

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