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Important Discovery Exposes Autoimmune Nature of ME/CFS - HERVs Implicated

Discussion in 'Phoenix Rising Articles' started by Phoenix Rising Team, Feb 20, 2013.

  1. Gijs

    Gijs Senior Member

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    In addition, I think that researchers like Lombardi and the WPI after the XMRV debacle not be taken seriously. I hope for those researchers that at least the research is carried out professionally this time. This model (HERV) does not explain the symptoms and findings by other researchers. How and what is infected in de nervous system that explains the chronic overstimulated autonomic part or the abnormal stressrespons by (HERV). It makes no sense. I am not so optimistic. It is one of the many abnormalities.
  2. snowathlete

    snowathlete

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    Thanks Mya, glad you liked it.
    Good questions!
    1. In short; yes. But, we dont know exactly what is happening here yet. If something is not right with the pDCs then that will affect a lot of the other immune cells in consequnce.
    2. Maybe. It would explain a lot wouldn't it.
    3. Um. HIV immunity isn't my area of knowledge - however, I am aware that people with HIV have higher HERV proteins, and researchers are wondering if they can use this as a means of targeting HIV. The problem with HIV (well not the only problem, obviously...) is that it mutates so rapidly so therapys to kill it dont work. The hope is the they may be able to target HIV via the HERV proteins. I dont know the specifics of that, but I read something along those lines.

    To elaborate more on your question - I wonder (and this is speculation) whether HERVs in our genome is not really a random accident, but rather some kind of positive mechanism to pass on information on viruses to the next generation, to help with immunity.
    SOC and merylg like this.
  3. lansbergen

    lansbergen Senior Member

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    It fits my hypothese and can be caused by the pathogen I always suppected. Still no test for that pathogen for living patients.

    For the record that is not herpes.
  4. lansbergen

    lansbergen Senior Member

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    Levemisole decreases autoantibodies in several diseases .

    I think if the causing pathogen can be eliminated the disease will vanish.
    merylg likes this.
  5. Gijs

    Gijs Senior Member

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    I know it is not herpes. But this researchers suggest that herpes 4 and 6 can be an important modulator of HERV-k18. Quote: ''Dr. Bridget Huber showed that HERV-K18 expression could be induced by herpes viruses such as Epstein-Barr virus and human herpes virus 6 (HHV-6) (34,61). Consistent with that work and with the data presented here, both of these viruses have been observed in the duodenum of individuals with ME (62)''. This is not correct according to recent research done by Komaroff et. al. Clin Infect Dis. 2013 Feb 13. [Epub ahead of print]
    Human Endogenous Retrovirus-K18 Superantigen Expression and Human Herpesvirus-6 and Human Herpesvirus-7 Viral Loads in Chronic Fatigue Patients.
    Oakes B, Hoagland-Henefield M, Komaroff AL, Erickson JL, Huber BT.
  6. snowathlete

    snowathlete

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    Thanks Val. Glad you liked it, and good idea telling friends and family. Most don't have time to read the whole paper and digest it, but it's worth them hearing about.

    You're more than welcome ana!

    Thanks tania. Those are big shoes to fill, so if I'm filling them, even in part, then that's praise indeed!
  7. snowathlete

    snowathlete

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    The Komaroff study was only looking at HERV-18 though, and only in the blood and saliva. It doesn't rule out other HERVs and it doesn't rule out the problem being in the gut - specifically the duodenum. It also didnt look for EBV (HHV-4), which surprised me - given the previous studies, why not look for that too?
    SOC likes this.
  8. Gijs

    Gijs Senior Member

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    The findings of Kenny et. al. are not specific to ME. These are also found in other diseases. This study again showed no breakthrough.
  9. acer2000

    acer2000 Senior Member

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    Maybe I'm missing something here. This is an interesting finding suggesting that HERVs may be present/activated in some people with symptoms of ME. But what does it have to do with auto-immunity?
  10. snowathlete

    snowathlete

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    Existing treatments tend to be about management and limiting damage by supressing the immune system. There are new treatments being developed for autoimmune diseases though that show promise. Here is an interesting article about just one of the many things that people are trying out in MS. This could work as a cure, in theory, though it is early days.

    It still is not well understood what triggers autoimmunity in the first place. If we understood that then we would be able to develop better treatments and maybe even cures, as well as preventative measures. One theory is that HERVs are involved and there is growing evidence for this. But it is complicated further because even if that is right, you then have to answer the question of what triggered the problem with the HERVs? One theory is that viruses might be that trigger, and some evidence has already been collected to show that EBV could be one such virus. The good thing is that depending on the actual mechanism, one finding in any one autoimmune disease could have positive implications for understanding other autoimmune diseases.

    Having an autoimmune disease would not be great, but it is better than having an autoimmune disease (or any other type of disease for that matter) and not knowing it, the illness being misunderstood and neglected etc.
    justy and Valentijn like this.
  11. Valentijn

    Valentijn Activity Level: 3

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    HERVs are present in everyone ... it's part of the human DNA. The issue is that we seem to have an immune reaction to a protein produced by HERVs. Since it's part of our DNA, reacting to it would be auto-immune.
    jimells and justy like this.
  12. Ema

    Ema Senior Member

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    There is some (limited) evidence and ongoing studies using IgG therapy to reverse autoimmune conditions. Many of the people I know on Hizentra (sub Q IgG) have had substantial reductions in the number of autoantibodies present.

    The doses used are generally higher than for IgG replacement therapy. And of course, since it is not FDA approved for this purpose, generally impossible to get from a financial standpoint unless you have a concurrent primary immunodeficiency disease (which is not out of the realm of possibility for many of us). I was luckily able to qualify for Hizentra through their patient assistance program.

    Ema
  13. Legolas

    Legolas

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    I gonna quote from the article;


    So the antibodies that you make to attack HERV proteins also (accidently) attack other cells/parts in the body.
    At least, this is how is see it.
  14. Leachim

    Leachim

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    Thank you, Joel, for a very well written article!

    As a comment to some of the comments: From what I know from different sources De Meirleir (I'm a patient of his) doesn't think this autoimmune reaction is the cause of ME, rather one of the later consequences of the disease process, the cause of disabling symptoms though, and probably also a factor in upholding the web of interacting pathological processes. De Meirleir's model of the disease process starts with disruptions in the gut flora causing an array of immune dysfunctions, and I suppose the autoimmunity should be one of the consequences of some parts of the immune system being hyperactive (parts of the innate immune system and Th2/the b-cells).
    snowathlete likes this.
  15. Gijs

    Gijs Senior Member

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    The immune system is hyperactive because the stressrepons or autonomic nervous system is hyperactive; (nor) adrenaline-cortisol-immune system etc... the problem is in the CNS. NOT DUE TO PSYCHOSOCIAL STRESS BUT BECAUSE THE SYSTEM IS BROKEN.
  16. Forebearance

    Forebearance Senior Member

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    I don't understand what this means:
    "The paper reports that the Plasmacytoid dendritic cells (pDCs) of eight out of 12 ME/CFS patients studied were found to be immunoreactive to antibodies against HERV proteins. "

    What does it mean to be immunoreactive to antibodies against HERV proteins?
    Can someone put it into plainer English for me?
    Thank you!!!

    Also, I wonder how this study would relate to Dr. Jamie Deckoff-Jones' theory that we are getting retrovirus fragments from vaccines which are completing or activating HERVs. Apologies to her if I'm not stating her theory correctly.
  17. snowathlete

    snowathlete

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    Hi Forebearance, I should have gone over this in the article really, sorry.
    What they did was Immunohistochemistry. You can read about that here on wikipedia. They apply a solution of antibodies (in this case HERV antibodies) to the tissue and they have been conjugated with enzymes that show up a color if there is a reaction (if the antibodies find the expected antigen that they are looking for (in this case HERVs). You can see in the actual paper the photographs of the tissue with colored cells where it has reacted (pages 4, 5 and 6).

    The vaccine link is an interesting one. Not sure but its potentially possible. Its widely accepted (i think) that we do have antibodies to various animal tissue in our bodies as a result of medications and vaccines developed using animals. Doesn't get talked about much for some reason. I always thought it was quite remarkable!
    Valentijn likes this.
  18. Sushi

    Sushi Moderator and Senior Member Albuquerque

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    I can't add to the scientific discussion but just want to thank Joel for writing this article. It is very helpful when you put it along side the published article. So Thanks! :thumbsup:

    Sushi
    Valentijn and snowathlete like this.
  19. liquid sky

    liquid sky Senior Member

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    Where can you obtain Levamisole, lansbergen? I know it is used to treat worms in animals, but I have not been able to find it anywhere.
  20. serg1942

    serg1942 Senior Member

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    Hello to everybody,
    As many of you, I'm trying to fully understand the mechanism proposed in the recent publish paper from KDM et al.

    I've read all your comments and reports, and they are great, but they seem not to address a few issues that for me, are the most important things to understand. So, I am going to write down the questions that I am not able to solve, with the target of being able to explain in very simple words the proposed mechanism, mainly for the Spanish CFS community, who mostly does not manage in English, and are eager to know what is all this about.
    The whole study is very well summarized here:

    http://phoenixrising.me/archives/16017
    (thank you Joel for the great article!)

    Questions:
    My goal is to complete /correct the following sketch:
    http://www.sfc-em-investigacion.com/download/file.php?id=236&mode=view
    (it's just an ugly-fast made drawing I made while reading the article and researching, but it'll be "nicer" when finished! :)

    pDCells express HERVs genome, transcribing HERVs' proteins (gag and env). They don't say, but I assume that they go to the cytoplasm after being transcribed, where they may act as superantigents, that after being processed by phagocytosis will create the HLA-DR (MHC II) membrane receptor, that distinguishes the Antigen Presenting Cells from the rest (APCs). But this process is carried out in an abnormal way, so that the Lymphocytes T that stick onto these receptors in order to be activated, and thus are"told" what antigen to attack, are improperly and non-specifically activated. A lot of lymphocytes are activated by this way, then they activate in turn lymphocytes B that will synthesize antibodies against HERVs's proteins.
    2- Where do these antibodies go?:

    a- To the cell membrane of the pDCs? If so, do they die, or are just wrecked as a response, b/c the lymphocytes attacking those antibodies are not efficient due to the "non-especific activation"? The immunohistochemical assay shows that only pDCs shown reactivity against HERV proteins, so the only way this can happen (that I know), is if in their membrane, they express antibodies against HERV proteins. To my knowledge, this may happen independently of whether gaga and env proteins are only inside the cell or also in the serum.

    b- To the HERV proteins, provided they go out of the cell. Do they? this is important in the sense that these proteins could travel throughout the whole body, so, they could be attacked in any place, explaining a systemic immune activation: systemic inflammation, coming from the gut! (this is the main idea...).

    c- To ANY free protein in serum or inside cells that resembles the HERVs' proteins. This is the basis of molecular mimicry, and this is actually the way that it's proposed for the origin of autoimmunity, that is, lymphocytes and other members of the acquired response would attacked self proteins or self cells, in ANY part of the body.

    Moreover, if we have a bunch of Lymphocytes "trained" to attack ANYTHING with antobodies against HERVs' proteins, they would attack ANY cell expressing these proteins...

    So, in short, based on the above, this is my main question:

    Where do the antibodies against HERVs' proteins go?, and what would be the exact process by which they are responsible for the autoimmunity? (Some of the possibilities I have listed above? A combination?)

    2- Last question: they explain that the humoral response (Th2) against the HERVs' proteins leads to autoimmunity through molecular mimicry. Ok, the process I have described, if I have got it correctly would be exactly this, what would explain a shift of Th1 to Th2. So then, we would have two pathways that could cause symptomatology:

    - Deffective Th1 response b/c of improperly activated lymphocytes T, and
    - Excess Th2 response by the process I've explained of molecular mimicry involving antibodies anti- HERV proteins, and directly by the effect of dysrupted pDCs: low NKs, inflamation, etc.

    So, the last quesion: What are the mechanism that wrecks the normal function of pDCs in the first place? I have assumed there may be two ways: 1- the improper Antigen Presentation process and 2- the attack of pDCs by lymphocytes.

    I would really appreciate if any of you could help me with all this questions. More than one brain think better than only one (especially if layman and brain fogged!).

    I, of course, do not have the knowledge to understand all this on my own, and would like to apologize beforehand for taking the risk of trying to understand things that are beyond my knowledge (that's why I'm asking to more expert people).

    Thanks in advance for your insights!
    Sergio

    PS. I'm a CFS patient myself, student of medicine, vice-president of a National spanish association of people affected by mercury from amalgam fillings (including many PWCFS), and collaborator with many ME/CFS associations and institutions.

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