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XMRV CFS UK study #II

Discussion in 'XMRV Research and Replication Studies' started by Orla, Feb 15, 2010.

  1. Gerwyn

    Gerwyn Guest

    The English studies are a bit like the following scenario

    You are given a persons home address-you want to find this person so as a first step you try looking for this person at a different address

    When you are not successful there ,as a second step you decide to try the pub(bar) across the road.You then spend ages arguing that you used the right map and it was the persons fault for not being there!
     
  2. oerganix

    oerganix Senior Member

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    And then when you can't find them, you announce that they don't exist.
     
  3. usedtobeperkytina

    usedtobeperkytina Senior Member

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    I remember reading that it is easier to get published if you disprove something or if your results are negative than if your study finds something new.

    When the WPI study came out, the critics jumped forward to find fault. Now, why? Why such suspicion? Why did Reeves make his biased comment? Why didn't he say, "This is exciting news, although we caution that future studies will need to confirm these findings before any conclusions can be drawn."

    And it wasn't just him that jumped to find fault. As was said, someone said, "You must have included people with other illnesses, such as cancer." The thought here is, "Ok, so the virus exists in sick people, but I don't believe it exists in CFS people." Why is it easier to believe XMRV can cause lymphoma than it is to believe it can cause CFS? And WPI did answer that accusation that they did not include lymphoma patients. (maybe they were removed, that is they were included by taken out of the final results numbers, that is disqualified in the end.)

    And then it was, "You didn't define the cohort clearly in the report." This is the one that is still hanging out there. "You didn't give enough detail of how you did it."

    You would think it would be easier to get a study published if it said, "I found something new, I saw it."
    Instead it is easier to get this published, "I looked for it, I can't find it. So it doesn't exist." Seems pretty clear the chance of "it" being there and hiding or his just missing "it" is much more plausible than that the first guy didn't see what he thought he saw.

    Tina
     
  4. Cort

    Cort Phoenix Rising Founder

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    THe problem is that CFS is very diverse -we can see that on the forums - people respond to different treatments and have different test results - so the idea that a single virus is responsible for that is controversial in the research world. They don't think diseases like that have a single virus connection because they haven't in the past. I don't have a problem with them saying that; they actually say that about a variety of chronic disorders. If CFS was confined to one organ that would be different.

    This doesn't mean that there isn't a connection; researchers theories are disproved all the time. (My pet idea is that CFS is a deep brain disorder and when you have problems that deep in the brain they can manifest themselves in many varying ways. I don't see why a central nervous infection couldn't cause a wide variety of problems). If XMRV was found in the majority of CFS patients I would think this would mean that it HAVE to be found in other disorders as well because I think we leap the boundaries alot.
     
  5. Cort

    Cort Phoenix Rising Founder

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    The problem for me is that I don't understand why Kerr - who is an exacting researcher (he splatted all over the CDC for their inexacting gene expression techniques) - would sign onto a such flawed study.
     
  6. Hope123

    Hope123 Senior Member

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    In most of science, it's actually the opposite: harder to get something published when you have a negative finding. In fact, when scientists want to review a topic throughly, they often do a thorough search of biblios and call up people in the field to make sure they aren't missing papers, abstracts, findings that were not published. The link between CFS and viruses was controversial to begin with and there is a long history of attempting to link viruses to various chronic illnesses (including MS) without solid findings so in this case, negative studies were viewed just as interesting as positive. A statistical method to assess publication bias when looking at mutliple studies is a funnel plot:

    http://en.wikipedia.org/wiki/Funnel_plot

    Right now there are too few studies to do this with on CFS.

    In regards to how diverse CFS is or isn't, whenever I'm ready to conclude that it's several diseases, I remind myself of TB/ Syphilis/ HIV/ lupus, each of which were know as "the great imitators" in their era becasue they could manifest in so many different ways. I think WPI has stepped over the line by linking XMRV to atypical MS, FM, autism, etc. with less than 50 that I know of tested in each group but in terms of CFS, the jury is still out for me about whether it's one illness or several.
     
  7. gracenote

    gracenote All shall be well . . .

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    Cort,

    When thinking about HIV and AIDS, would you still say the above?
     
  8. cfs since 1998

    cfs since 1998 *****

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    It's only controversial with people like Reeves and Wessely and people who are ignorant about what ME/CFS is. It shouldn't be a far-fetched idea at all among the real ME/CFS researchers, in fact it is the most logical hypothesis.
     
  9. julius

    julius Watchoo lookin' at?

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    Canada
  10. natasa778

    natasa778 Senior Member

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    Because admitting that would mean admitting the depths of their ignorance about CFS/fibro/autism etc.

    This all reminds me of the Perfectly Normal Best, from Hitchhikers Guide to the Galaxy: ...The Perfectly Normal Beast is a buffalo-like creature. They appear out of nowhere and sweep in their thousands across the plains in a stampede that lasts six days and, well, disappear again just as mysteriously as they appeared. And then, in Spring, they do it again but in the other direction… No-one really knew where they came from and … nobody ever really bothered to ask. I think they call them perfectly normal beasts because otherwise they might think it's a bit odd. This way there is nothing unusual about the perfectly normal beast;...
     
  11. usedtobeperkytina

    usedtobeperkytina Senior Member

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    Yet, given the fact that XMRV can infect multiple cells in multiple systems, and could affect CNS with multiple symptoms, then it is plausible that it is the cause of all true CFS. Even with other triggers, mold, etc, XMRV could be the difference between who gets CFS of those exposed and who doesn't.

    As in GWS, not everyone got sick. While other factors could make the difference, an underlying retrovirus in the immune system is also possible.

    Tina
     
  12. oerganix

    oerganix Senior Member

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  13. julius

    julius Watchoo lookin' at?

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    Personally, I think it fits too. I was just responding to CFSsince, just as a clarification that it's not only Wessely and Reeves and their ilk.
     
  14. Cort

    Cort Phoenix Rising Founder

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    I think it can fit too. Its just that my understanding is that CFS ( except for AIDS) would be the first disease in which something like this happened. Where you had a kind of large variable disorder that was strongly tied to one pathogen. It would open peoples eyes. IT would be a pretty new thing I believe.
     
  15. Gerwyn

    Gerwyn Guest

    To be fair i think that is what a lot of drs have problems with.It goes against their training having such an apparently bewildering array of symptoms with a single causative aetiology.It would be the second retrovirus known to cause these symptoms though.
     
  16. lansbergen

    lansbergen Senior Member

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    What about other mammalians?

    Feline Leukemia Virus in cats?

    It can cause:
    * Weight loss
    * Fever
    * Immunodeficiency and infections
    * Anemia
    * Immune-mediated diseases
    * Reproductive problems
    * Gastrointestinal disease
    * Neurologic disease
    * Platelet disorders
    * Lymphadenopathy (enlarged lymph nodes)
    * Cancer
    * Respiratory and eye problems
    * Oral disease
     
  17. Gerwyn

    Gerwyn Guest

    very goog point do you know about primates
     
  18. lansbergen

    lansbergen Senior Member

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    There are no indications Feline Leukemia Virus is a zoonose.

    I have no idee whether it can infect other primates.
     
  19. natasa778

    natasa778 Senior Member

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    SIV in primates. I've got tons of stuff relating to neurological dysfunction, no reason why all other boxes would not be ticked:

    SIV model of neuroaids

    http://www.scripps.edu/mind/fox/research.html



    J Neurovirol. 2008 Aug;14(4):301-8.

    Behavioral and neurophysiological hallmarks of simian immunodeficiency virus infection in macaque monkeys.

    Cheney PD, Riazi M, Marcario JM.Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas 66160-7185, USA. pcheney@kumc.edu
    Macaque monkeys infected with various neurovirulent forms of simian immunodeficiency virus (SIV) represent highly effective models, not only of systemic acquired immunodeficiency virus (AIDS), but also neuroAIDS. Behavioral studies with this model have clearly established that SIV-infected monkeys show both cognitive and motor impairments resembling those that have been reported in human immunodeficiency virus (HIV)-infected humans. This paper combines data from a number of behavioral studies in SIV-infected macaque monkeys to obtain an overall estimate of the frequency of impairments in various motor and cognitive domains. The results were then compared to similar data from studies of HIV-infected humans. Whereas cognitive functions are most commonly impaired in HIV-infected humans, motor function is the domain most commonly impaired in SIV-infected monkeys. Electrophysiological studies in SIV-infected macaques have revealed deficits in motor-, somatosensory-, visual-, and auditory-evoked potentials that also resemble abnormalities in human HIV infection. Abnormalities in motor-evoked potentials were among the most common evoked potential deficits observed. Although differences in behavioral profiles of human HIV disease and SIV disease in monkeys exist, the results, nevertheless, provide strong validation for the use of macaque models for translational studies of the virology, immunology, pathophysiology, and treatment of neuroAIDS.PMID: 18780231

    ....Significant correlations were found between impaired performance on the bimanual motor test and axonal damage (accumulation of beta-amyloid precursor protein in the corpus callosum) as well as increased microglial activation and macrophage infiltration (levels of CD68 and Ham56 immunostaining). These results suggest that axonal damage is related to the behavioral impairment induced by infection with SIV. The axonal damage may result from neuroimmune responses, including microglial and macrophage activation. Therefore, axonal damage may be a morphologic manifestation of neuronal dysfunction that underlies development of behavioral impairment in HIV/SIV CNS infection. PMID: 12907390

    This model provides outstanding opportunities to delineate the pathogenesis of infection, to study the regulation of virus gene expression, and to identify host immune responses throughout the acute, clinically silent and late stages of infection. Using this model, the authors have demonstrated that the virus enters the brain within days after inoculation, that CCL2 (monocyte chemoattractant protein [MCP]-1) plays a major role in recruiting monocytes/macrophages to the brain, and that type I interferons are critical in suppressing early virus replication and inducing viral latency. This model provides a rigorous platform for the testing of potential antiretroviral, immune reconstituting, and/or neuroprotective agents and already has been used to confirm the neuroprotective properties of minocycline, which now is being tested in clinical trials of HIV-infected individuals. PMID: 18780232


    Gerwyn you'll love this one:

    ... STUDY DESIGN/METHODS: Cognitive and motor function was assessed in rhesus macaque monkeys infected with simian immunodeficiency virus (SIV). In situ hybridization, immunohistochemistry, and quantitative image analysis were employed to assess the relations among productive infection, NO synthase (iNOS), and dendritic injury. RESULTS: Productive infection of cells of the macrophage lineage in CNS is associated with inflammation, increased expression of iNOS, and dendritic injury. The tests of cognitive and motor function employed were abnormal in both animals that had evidence of productive infection and those that did not. CONCLUSIONS: Increased NO accompanying productive infection and encephalitis may be one cause of neuronal injury in lentivirus infections of the CNS. Extension of tests of cognitive and motor function to late-stage AIDS in rhesus monkeys is needed to assess the potential role of NO-induced dendritic damage in lentiviral encephalopathy/AIDS dementia complex. PMID: 10413365
     
  20. cfs since 1998

    cfs since 1998 *****

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    Why are you calling it a "disorder"? Isn't that Reeves used to say... "CFS is not a disease, it's a disorder." I call it a disease. One pathogen explaining ME/CFS would not be surprising one bit, evidence has been building for 25 years that (a) virus(es) are involved.
     

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