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HERV in MS - clinical trial

Discussion in 'Other Health News and Research' started by Daffodil, Oct 10, 2013.

  1. Daffodil

    Daffodil Senior Member

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  2. merylg

    merylg Senior Member

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  3. August59

    August59 Daughters High School Graduation

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    This might end up being interesting if I can understand it! Thanks for the info.
     
  4. Legendrew

    Legendrew Content team

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    Considering the vast, vast majority of people have these I do wonder why HERVs receive so much attention. It is highly questionable whether there is an immune response targeted towards there HERVs and if there is I think the true question would be why the immune response is suddenly targeting non-functional proteins proteins produced by otherwise inert stretches of genetic material.
     
  5. Bob

    Bob

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    I haven't studied this subject in detail, but it is said that some HERVs can express partial viral particles (i.e. proteins). Perhaps the protein expression differs in people depending on genetics or environmental factors?
     
  6. natasa778

    natasa778 Senior Member

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    Raltegravir (Isentress) is also currently being trialled for MS. There are long-ish threads on both of these trials on this forum, with lots more details and links...
     
  7. anciendaze

    anciendaze Senior Member

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    Bob, I'd like you to consider the state of some HERVs, while none are known to be active as inherited in humans, there are many full-length retroviral genomes. (In the case of HERV-K111 we are still sorting out just how many have been overlooked.)

    The most common way in which full-length retroviral genes in HERVs are inactivated is by misplaced stop codons, frame shifts are also prevalent. If you were to design a "patch" to correct this it would only need to contain a few base pairs, though you would want a longer sequence to see that it matched up correctly with surrounding sequences. It is apparent there are many ways to cause transcription of HERVs, so that is not a problem. All you need to do is fix those small errors. Similar errors do not prevent diseases in animal models as with MMTV or JSRV. A helper virus supplies the missing base pairs or gene functions. The virus can be described as both an ERV and an exogenous virus. This is much easier to observe in animals with short life cycles, where viral replication is rapid, than it is in humans.

    I would be far more surprised if nature overlooked the option of supplying just enough information to transcribe and reactivate these proviruses than I would be to learn that this also takes place in humans. Those cells are behaving as if they are fighting viral infection. Why not treat it as if this were a viral infection? The fact that a process does not satisfy academic definitions of viral infection means much less to nature than to academic researchers.
     
  8. Bob

    Bob

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    I have a feeling that there is a heck of a lot that we don't yet know about HERVs, and that this field of research is in its infancy. I should do some deeper reading on it one day. I think it will be interesting.
     
  9. anciendaze

    anciendaze Senior Member

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    Bob, I apologize for directing a response to you, when I meant Legendrew. The old short-term memory failure for names strikes again!

    While I'm posting, I want to make it clear that I won't be astonished if this particular trial intervention fails. Even if a process closely resembling a retroviral infection is taking place, finding a good way to interrupt it will not be easy. This is likely to take a great deal of trial and error. Even when we can clearly identify a retrovirus like HIV or HTML, it is very difficult to reverse the pathology. We feel lucky to have arrested deterioration for many patients.
     
    natasa778 and Bob like this.
  10. Daffodil

    Daffodil Senior Member

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    yes it will likely be a lot more complicated than just taking an antiretroviral. many HIV patients on HAART still have lupus and other autoimmune diseases.

    also, we may need some HERV expression so we might have to find a way to selectively silence the proteins we don't want expressed..?

    personally, even though AZT was helping, it only helped at a higher dose which I could not tolerate for long....so success might be dose-dependant, especially for late-stage patients.

    since the monoclonal antibody targets only the offending(?) proteins, that one seems more interesting to me.

    GeNeuro was supposed to know if their drug halted or reversed MS lesions in the 6-month follow-up, by September....but I cannot find any announcements.

    Legend...I had the exact same opinion and indeed, so does my infectious disease specialist, who is an HIV expert.....but DeMeirleir/Lombardi did next generation sequencing on 2 samples of duodenum tissue of CFS patients (small number I know)....and they did not find any virus...only evidence of HERV activaton (and not in controls).
     

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