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Looking for MuLV's and how they cured them in mice...

Discussion in 'XMRV Research and Replication Studies' started by Impish, Aug 27, 2010.

  1. Impish

    Impish Senior Member

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    Victoria, BC
    So far in the distant past it seems like someone did for looking for MuLV's in humans...

    http://www.cancer-therapy.org/CT6A/HTML/31._Gardner,_285-302.html

    Too bad they didn't find them then.

    They did find how to cure them in mice:

    Contrary to expectations based on the AKR mouse model, control of MuLV and prevention of lymphoma and paralytic disease in the high MuLV expressor LC mice was dramatically accomplished, as mentioned above, by foster nursing on virus-free NIH Swiss mothers (Gardner et al, 1979). Surgical removal of the spleen, the virus factory early in life, lowered the virus burden sufficiently to prevent the CNS disease completely and markedly reduced the incidence of lymphoma. Passive immunization of newborn LC mice with goat immunoglobulin, having a high neutralization titer to ecotropic virus and a low titer to amphotropic virus, completely prevented the paralytic diseases but only slightly lowered the incidence of lymphoma (Gardner et al, 1980b). Active immunization with inactivated LC MuLV had no effect, of course, in already infected immune tolerant LC mice, although they responded well to a heterologous MuLV vaccine and other foreign antigens (Klement, 1976). A decade later, the beneficial effect of transplacental anti-retroviral therapy with azidothymidine was shown in lab mice that were protected against the CNS disease after inoculation with LC ecotropic MuLV during mid-gestation or at birth (Sharpe et al, 1987). This is the first example of successful antiviral therapy for congenitally transmitted retrovirus. Finally, selective breeding could strongly suppress LC-MuLV. Because the MuLV of LC and other wild mice is N-tropic, i.e. grows preferentially in NIH Swiss mouse cells, and not in BALB-C mouse cells (B-tropic), introduction of the FV-1B virus resistance gene from C57 BL-10 inbred mice completely blocked LC MuLV expression in the F-1 hybrids (Gardner et al, 1976b)
     
  2. Impish

    Impish Senior Member

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    In case anyone is wondering azidothymidine = AZT which was found to be the best at repressing XMRV I believe.
     
  3. omerbasket

    omerbasket Senior Member

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    Impish, in vitro Raltegravir was found best against XMRV, and than AZT (correct me if I'm wrong).

    Anyway, I think that as a non-scientist I understands much better studies that would seem to other non-scientists (who are not interested in science) like ancient Chinese, but I must say that this abstract looks to me at least like modern Chinese.

    I anyone would be willing to translate it to simple words and meanings, it would be great.

    Anway - It seems to me that they couldn't cure mice that are infected with MuLV's, just prevent diseases (again, correct me if I'm wrong here). And that's a big one, because if we are in some way contagious, or even just thought to be contagious, there would probably be a big difference for us between "being completely functioning, but XMRV positive and contagious" and "being completely functioning, and not with XMRV anymore - therefore, not contagious at all".
     
  4. Daffodil

    Daffodil Senior Member

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    yes they were able to prevent the mice from becoming infected, not cure the infection.
     
  5. Impish

    Impish Senior Member

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    Sorry... I could have done some translating here.

    The parts I found interesting is that they mentioned the spleen as a "virus factory" which suggests a place to look for MuLV in humans. They also mention using immunoglobulin which has been suggested as a treatment in humans due to the immune system imbalances detected. This seems interesting in that it supports a proposed treatment in humans based on what has been observed in mice. It also provides support for the fact that MulV's are causing CFS in that similar immune system problems were found in mice.

    It also mentions that anti-retroviral's worked to protect the mice from the CNS disease associated with MuLV's. Interesting that MuLV's cause a CNS disease in mice again suggesting that they are on the right track with MuLV's = CFS. The fact that anti-retroviral's worked in mice again provides an animal model backing up what has been observed in humans taking them. Obviously it will be interesting to see what strains are affected.

    Finally it is interesting in the article that they found MuLV's in clusters (like CFS). They also found that some mice don't get it due to genetic reasons. I REALLY REALLY think getting 23 and me involved with CFS would be of great interest. Since we know what gene's protect mice we should be able to look for similar gene's (or the lack thereof) in humans and relatives with CFS. That would provide absolute proof (IMHO) that MuLV's are causing CFS.
     
  6. omerbasket

    omerbasket Senior Member

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    Thanks a lot, Impish.
     
  7. Wonko

    Wonko Senior Member

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    The other side.
    hmmm...the NHS wont give me immunoglobulin or antiretrovirals - and it appears as I apparently do use my spleen removal may not be an option either - at least on the NHS (lol)

    so I guess I'm still going to have M.E. next week......
     
  8. Rrrr

    Rrrr Senior Member

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    excellent find! and great points you mad in yr #5 post!

    i was particularly interested this quote from the same paper we are currently discussing (http://www.cancer-therapy.org/CT6A/H...,_285-302.html): "introduction of the FV-1B virus resistance gene from C57 BL-10 inbred mice completely blocked LC MuLV expression in the F-1 hybrids (Gardner et al, 1976b)"

    so that means that if we can get stem cells from someone with FV-1B virus resistant gene, we may be able to block some of the MuLV? would this be like blocking the CCR5 gene in HIV patients?
     

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