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Dr Martin Lerner's abortive infection theory of ME/CFS — Unifying herpesvirus & enterovirus ME/CFS?

Discussion in 'Latest ME/CFS Research' started by Hip, Nov 8, 2017.

  1. Hip

    Hip Senior Member

    I am going to answer your above quoted question in this thread, which is a more appropriate place.

    There is not much evidence to substantiate Martin Lerner's theory of abortive herpesvirus infections in ME/CFS (but there is good evidence to substantiate a very similar phenomenon called non-cytolytic infection in the case of enterovirus-associated ME/CFS).

    It's not the immune system as such which prevents the virus from completing its replication cycle; rather abortive infection is due to the virus entering the wrong sort of human cells — cells which do not possess the right internal conditions to facilitate full viral replication (these wrong sort of cells are called non-permissive cells).

    Abortive infection has been observed in cell line experiments in vitro: if you use a cell line of cells that are non-permissive for EBV, you can observe an abortive infection. I am not sure if herpesvirus abortive infections have been observed in vivo. Certainly though HIV abortive infections are known to occur in vivo.
    used_to_race likes this.
  2. JeanneD

    JeanneD Senior Member

    Take this with a grain of salt as it was a long time ago, so I might have got it mixed up with something else in the ensuing years, or I might have not understood correctly.

    IIRC, Dr Lerner got miffed when people called the early rough rxns to Valcyte herxing. It is definitely not herxing. That doesn't happen with viral infections. He speculated that in many of his patients, their immune system has been reacting unsuccessfully to the abortive infections for so long that their immune systems (to put it in layman's terms, not medical terms) got worn out or gave up trying to fight it. Once the Valcyte slowed the abortive infection, the immune system recognized it could now fight back and came back online with a vengence, maybe over-reacting. Valcyte rxns in ME patients look like strong immune rxns -- like a very bad flu. That certainly fit my experience.

    My daughter had no side effects from Valcyte while I had a pretty bad one (worth it though, given how much I improved). The speculation is that my daughter's younger immune system and less severe illness for less time kept her immune system from "giving up" while my older, more challenged immune system was exhausted and so when it got help from Valcyte, the response was much greater.

    As long as we saw Dr Lerner, he did no immune testing, so he never tested this idea to my knowledge. It was just a speculation on his part.

    Later, when we switched specialists and got immune testing, my immune system was more out-of-whack than my daughter's, although we both had abnormalities.
    bspg, pattismith and Hip like this.
  3. imitate-past-reign


    Note that only one a million B-cells is infected with EBV at all, while native T-cell dysregulation (the genetic / environmental component) causes less clearance within the CNS compartment of EBV and proliferation of even uninfected B-cells. This is why Rituximab is not the greatest monotherapy. Clearance of EBV by Rituximab is almost always in concert with CHOP chemotherapy.

    Moreover, Rituximab is always taken with high-potency glucocorticoids which further dysregulate this system.

    It is not unreasonable to suggest that 1% of the population will have permanent sequelae from EBV/CMV infectious mononucleosis, and that would present as obvious Chronic Fatigue syndrome, regardless of the semantic arguments about the lytic cycle.

    The EBV / CMV connection is fine, but why are the treatments is a derivative of acyclovir from the early 1980s?

    - Autologous Natural Killer Cell adoptive immunotherapy
    - Autologous T-Cells against EBV
    - CMV- and EBV-specific immunoglobulins

    Why is the leading theory for CFS a shoehorned autism trial that was poorly blinded, using an IV-drug with a terrible therapeutic index requiring repeated dosing, using a biochem 101 theory about energy production?

    Especially when none of the above have been tried.
    pibee likes this.
  4. rodgergrummidge

    rodgergrummidge Senior Member

    welcome to PR @imitate-past-reign

    Perhaps there was a typo in your above comment? Are you suggesting that Autologous Natural Killer Cell adoptive immunotherapy, Autologous T-Cells against EBV, CMV- and EBV-specific immunoglobulins would be better treatments for EBV-induced CFS than antivirals? Or the other way around? Which IV-drug were you making a comparison to? Ritux?

  5. imitate-past-reign


    Thanks for your welcome to the forum. I’m on my phone so this isn’t as lucid as normal. Sorry for the mix-up - yes, I’m glad Valcyte works for some but it is crude (both adverse and efficacy) and expensive.

    Roger, I was referring to suramin. The leading candidates for treatment in CFS are cyclophosphamide and suramin I suppose. That’s pretty dire in terms of innovation.

    Cyclophosphamide diminishes the t and B cell response which goes against the framework here. I am really underselling how terrible an idea that is, but it might actually improve immune antibody type patients (women over 30 post-natal).

    In klimas et al. 2001 they removed the patients lymph nodes under anesthesia, expanded, replaced them under anesthesia. Trial was moderately successful - trial sponsor pursued other applications.

    They didn’t need to undergo surgery, you just draw blood, expand the t-cells, re-injection.

    The question I would have to be to those who control private funding for immunotherapeutic treatment like this is - “Do you have a better idea?” And if they do, it’s great for all of us.
    Helen and TracyD like this.

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