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ME symptoms are due to learned responses by B and T cells

Discussion in 'Latest ME/CFS Research' started by Jenny, Dec 21, 2012.

  1. Jenny

    Jenny Senior Member

    Not sure if this has been posted previously....

    Can persistent Epstein–Barr virus infection induce chronic fatigue syndrome as a Pavlov reflex of the immune response?


    Elena Agliariab*, Adriano Barracd, Kristian Gervasi Vidale &Francesco Guerracf
    pages 740-762

    Publishing models and article dates explained
    Received: 24 Nov 2011
    Accepted: 13 Jun 2012
    Version of record first published: 16 Jul 2012
    Article Views: 664​

    Chronic fatigue syndrome is a protracted illness condition (lasting even years) appearing with strong flu symptoms and systemic defiances by the immune system. Here, by means of statistical mechanics techniques, we study the most widely accepted picture for its genesis, namely a persistent acute mononucleosis infection, and we show how such infection may drive the immune system towards an out-of-equilibrium metastable state displaying chronic activation of both humoral and cellular responses (a state of full inflammation without a direct ‘causes–effect’ reason). By exploiting a bridge with a neural scenario, we mirror killer lymphocytes TK and B cells to neurons and helper lymphocytes [​IMG] and [​IMG] to synapses, hence showing that the immune system may experience the Pavlov conditional reflex phenomenon: if the exposition to a stimulus (Epstein–Barr virus antigens) lasts for too long, strong internal correlations among B,TK and TH may develop ultimately resulting in a persistent activation even though the stimulus itself is removed. These outcomes are corroborated by several experimental findings.
  2. Snow Leopard

    Snow Leopard Hibernating

    South Australia
    Interesting, I had wondered about this sort of approach. I'll have to get one of my more mathematical friends to explain it to me.

    While this particular model is probably wrong (or incomplete), the answer may well be along these lines.
  3. alex3619

    alex3619 Senior Member

    Logan, Queensland, Australia of IiME Vol 3 Issue 1 Screen.pdf

    Scroll down to page 23. If this research is accurate then the supposition that the virus has gone could be wrong. First, herpes viruses reactivate, especially in patients with low killer cell function, which is common in ME. The enterovirus paper summarizes two additional viral life cycles. It has always been presumed that enterviruses follow the standard lytic lifecycle. Infect the cell, take over the cell, replicate like crazy, lyse the cell to release the new virus particles. Infect a new cell, repeat.

    The enterivirus paper shows the mechanism whereby enteroviruses can persist and infect cells without inducing viremia. Enteroviruses in effect have a stealth virus mode. This fits Chia's findings that nearly all of us have high tissues entervirus load. I supect, based on Lerner's findings of herpes viral particles and unusual antibodies to the interior of herpes viruses, that herpes viruses may do the same thing.

    Any model that presumes that the virus is gone may be invalid in ME now. It has been since at least 2009 but I think this was lost in the furore over XMRV. Any researcher who presumes a virus is not present due to lack of viremia, especially for enteroviruses (and possibly herpes viruses) is making an unfounded assumption.

    What we don't know is if this problem is coincidental (but a high association rate makes this unlikely) or opportunistic, or causal. Maybe this problem can only manifest under physiological conditions if the immune system is already defective, which would make these infections opportunistic. Or maybe the high tissue load with low viremia is what sets the whole ME physiological response in motion.

    The issue that similar particles are found with herpes viruses indicates that association is a poor fit, leaving opportunistic infection or causality.

    Bye, Alex
    Xandoff, heapsreal, SOC and 3 others like this.
  4. Enid

    Enid Senior Member

    Well it does seem to be very clear to us non-scientists that knock out and replacement/regrowth of immune system cells is not only a breakthrough but the way forward.
  5. Lynne B

    Lynne B Senior Member

    sydney, australia
  6. The model seems partially adequate but does not fit the observation that the incubation period of ME is 4-7 days. Rather than staying at 'this happens in some people, not in others', an additional factor is required: a trigger. I.e., persistent EBV (or another HHV) is central but by itself not enough to induce ME.
    Enid likes this.
  7. lansbergen

    lansbergen Senior Member

    The incubation period of the disease I have, is 7 to 10 days for the primary infection as well as reactivation/reinfection.
  8. xrayspex

    xrayspex Senior Member

    enid and lynne--how does one "knock out and replace"
  9. ukxmrv

    ukxmrv Senior Member

    Wasn't that one of the theories about using Rituximab?
  10. alex3619

    alex3619 Senior Member

    Logan, Queensland, Australia
    Hi, if ME is a multi-stage issue, then the incubation period for some of the epidemics might be for the trigger, and may not reflect causation. This is a presumption, it might be right, or it might be wrong, or it might be right for some and not others.

    Indeed there is a major potential confound here. Even the idea that the incubation period is, for example, 7 days, might be totally wrong. It rests on the single pathogen presumption. During incubation in say a 14 day pathogen, the immune system will start going haywire. Latent pathogens will reactivate. If those are responsible more than the current infection, then the "incubation" period may just be a reflect of the reactivation period for latent pathogens and the damage they do.

    The latent pathogen idea also explains why some people can get ME after injury, or toxic insult. The usual epidemic models don't.

    Personally, under current data I am aware of, I think that damage is critical. I want to know what the pathogen is doing at what stage. My guess is that ME arises after the gut mucosa is compromised, or the BBB is compromised, or even the heart is compromised. I think that is the real trigger for autoinflammatory changes, regardless of the pathogen invovled.

    What I would like to see are detailed prospective studies where healthy people in large numbers are tracked for a decade, and every infection is monitored very very closely. This would be good for other things beside ME research as well.

    Bye, Alex

    PS Another confound is this: while we know the incubation period for many pathogens the first time, do we really know the incubation period for reactivation of prior infections? Does the idea of an incubation period even make sense for these?
    merylg likes this.
  11. lansbergen

    lansbergen Senior Member

    The symptoms of the primary pathogenic in my case can be so summier most will miss it and when they are severe can be mistaken for flu.

    It was only because I was an experienced observer who was told to be alert for new zoonosis that I learned to recgonize it.

    Back then the pathogen I suspected was assumed to be a slow infection with no symptoms untill the point of no return was reached. Much research is done since then and the dogma is challenged by many.
  12. The incubation period is indicative for the trigger (enterovirus, presumably). That does not exclude other causalities. It seems perfectly fine to me to call the herpes virus the cause of ME even though you don't get the disease until it's triggered.

    I don't think it is possible for an injury to trigger ME.

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