The 12th Invest in ME Research Conference June, 2017, Part 2
MEMum presents the second article in a series of three about the recent 12th Invest In ME International Conference (IIMEC12) in London.
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Enterovirus-Induced ANT Autoantibodies: the Cause of ME/CFS?

Discussion in 'General ME/CFS Discussion' started by Hip, May 2, 2017.

  1. Hip

    Hip Senior Member

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    Enterovirus-Induced ANT Autoantibodies: the Cause of ME/CFS?

    Research beginning in the 1980s in Germany on enteroviral heart muscle infections (myocarditis) found evidence of an autoantibody which targets the adenine nucleotide translocator (ANT) protein located on the mitochondrial membrane, and thereby leads to impairment of mitochondrial energy production.

    The German researchers observed that these ANT autoantibodies are cross-reactive to enterovirus VP capsid protein of coxsackievirus B3.[1] So the researchers suggested that enterovirus may be inducing these autoantibodies by molecular mimicry, as a result of the viral VP capsid protein being molecularly similar to the ANT protein found on mitochondria. To support this claim, they also note that there are homologies in the peptide sequence of the ANT protein and the VP capsid protein of coxsackievirus B3 (such homologies are thought to underpin autoimmunity by molecular mimicry).[2]

    Because mitochondrial ANT protein plays a crucial role of transporting ATP generated in the mitochondria into the cytosol of the cell, as well as transporting ADP from the cytosol back into the mitochondria for recycling, any dysfunction in the ANT protein, caused by an autoantibody binding to ANT, could severely disrupt energy metabolism.

    And indeed, the German research found that in coxsackievirus B myocarditis and dilated cardiomyopathy (dilated cardiomyopathy is a further progression of myocarditis), there was a major disturbance in the energy metabolism in the heart muscle.[3][4]

    In fact in one guinea pig study, they found the measured energy output from hearts affected by the ANT autoantibody was five times less than the energy output from the hearts of healthy animals. And in addition, ANT autoantibody-affected hearts produced more than double the amount of lactate.[5] So clearly this ANT autoantibody is associated with a very substantial impediment in energy production, as well as increased lactate production. That certainly is beginning to sound like the state of affairs we find in ME/CFS.



    Implications of ANT Autoantibody Research for ME/CFS

    The ANT autoantibody research was noted by Professor Peter Behan of Glasgow University, Scotland, who suggested in a paper in 1985 that the ANT autoantibody might be involved in creating the low energy state of ME/CFS.[6] In others words, Prof Behan proposed the following viral-autoimmune etiology for ME/CFS:

    Enterovirus infection ➤ induces ANT autoantibodies ➤ disrupts mitochondria ➤ leads to ME/CFS

    Surprisingly, nobody to my knowledge has looked to see if ANT autoantibodies are present in ME/CFS, even though they are linked to enterovirus infections and cause a huge decrease in muscle energy production.

    However in recent years, evidence indicating the mitochondrial ANT protein is pretty dysfunctional in ME/CFS patients has emerged: the 2009 energy metabolism study of Myhill, Booth and McLaren-Howard (MBM) found that ME/CFS patients have major dysfunctions in their ANT protein — both dysfunctions in the ANT transport of ATP from the mitochondria into the cytosol of the cell, as well as dysfunctions in the ANT transport of ADP from the cytosol into the mitochondria.[7] Thus this MBM study implies that something is affecting ANT in ME/CFS patients. Could that something be ANT autoantibodies?

    Note that in the MBM study, they refer to the mitochondrial ANT protein as "translocator protein". This adenine nucleotide translocator (ANT) protein incidentally is also known by the names of: ATP/ADP translocator, or ATP/ADP carrier.

    Furthermore, Fluge and Mella's research, which found that rituximab can improve or cure ME/CFS, also suggests that an autoantibody may be driving ME/CFS. Rituximab deletes all the B-cells in the blood, and so some time after rituximab treatment, the production of autoantibodies will tend to cease. Thus the idea that ANT autoantibodies might be a cause of ME/CFS is consistent with observations that rituximab can improve or cure ME/CFS.



    ANT Autoantibodies and Calcium Channelopathies

    The German researchers found that their ANT autoantibody is also cross-reactive to the calcium channel, and that as this autoantibody binds to the calcium channel, it alters calcium influx into the cell, resulting in calcium channelopathies.[1][8] Recent research from Australia has now found calcium channelopathies in the natural killer cells of ME/CFS patients.[9] Perhaps an ANT autoantibody might help explain these ME/CFS channelopathies.



    Grand Unifying Theory of ME/CFS?

    This idea that ANT autoantibodies may be driving ME/CFS would tie together three characteristics of ME/CFS: its well-researched links to enteroviral infection; its apparent involvement of autoimmunity; and its observed energy metabolism dysfunctions. So this enterovirus-induced ANT autoantibody, if it exists in ME/CFS, could amount to a grand unifying theory of ME/CFS.



    If ME/CFS Were Caused by ANT Autoantibodies, What Would Be the Treatment?

    Obviously rituximab is a treatment that should eliminate ANT autoantibodies.

    And since these ANT autoantibodies appear to arise from a chronic enterovirus infection, elimination of that infection could also treat ME/CFS. Dr John Chia's interferon treatment of enterovirus infections in ME/CFS, which put some patients into remission for 2 to 14 months, indicates that treating enterovirus can be effective. Unfortunately interferon is not viable as a long term treatment, but its one-off efficacy does prove in principle that treating the virus treats ME/CFS.

    A third speculative approach that might help decrease the possible ANT autoantibodies in ME/CFS involves reducing the cytokine IL-17 and reducing the number of Th17 cells. A 2010 mouse study found that in acute coxsackievirus B3 myocarditis, reducing IL-17 led to a reduction in ANT autoantibodies, which the authors suggested could lead to a novel therapeutic approach for myocarditis.[10] Th17 cells are characterized by the production of IL-17, and in other myocarditis studies, Th17 cells have been linked to the worsening of coxsackievirus B myocarditis, because Th17 seems to promote viral replication.

    Thus a treatment which decreases Th17 and IL-17 may well reduce ANT autoantibody production. The supplement N-acetyl-glucosamine has been shown to reduce both Th17 and IL-17.[11] There are also several other drugs and supplements which are known to inhibit Th17 and IL-17.



    Further Details of the ANT Autoantibody Research

    In terms of how the ANT autoantibody can affect the functioning of the ANT protein on the mitochondrial membrane, the researchers have proposed four possible mechanisms:
    It's interesting that ANT protein is synthesized in the cytosol of the cell, and then later transported to the mitochondria. So the ANT autoantibodies could bind to the ANT protein while this protein is still in the cytosol.



    The researchers did try to verify that an antibody had entered the heart muscle cells:
    There are actually a number of anti-mitochondrial autoantibodies known, see: Anti-mitochondrial antibody. So it is not unusual to have autoantibodies that target parts of mitochondria.



    A further complexity about ANT protein is that the researchers found a shift in the relative expression of the three ANT protein isoforms (ANT1, ANT2 and ANT3) in myocarditis and dilated cardiomyopathy patients:
    This increase in ANT1 expression, incidentally, may be detrimental to patients with enterovirus (EV) myocarditis or dilated cardiomyopathy heart infections:
    So lowered ANT1 expression is linked to elimination of the enterovirus infection. The authors say that ANT1 overexpression influences the expression of other genes that may affect viral replication.

    Incidentally, if lowered ANT1 expression is associated with spontaneous elimination of enterovirus infection, then conceivably any treatment which reduces ANT1 expression might have useful antiviral effects.



    A Question I Have

    One question I have: why does this ANT autoantibody apparently induced by enteroviral heart muscle infection only affect the heart muscle, and not the other organs? The researchers found that in dilated cardiomyopathy patients, there was significant binding to heart ANT protein, whereas little or no binding was found on kidney ANT protein or liver ANT protein.[13] So the ill effects of the ANT autoantibody seem to be restricted to the heart.

    Although the enterovirus infection itself is located in the heart, I am not really clear why the ANT autoantibodies that this infection induces (which are manufactured by the B-cell-derived plasma cells in the blood circulation) do not also disrupt the ANT protein in the mitochondria of the cells of other organs in the body.

    Perhaps @Jonathan Edwards might know of a mechanism which keeps the autoimmune effects of ANT autoantibodies restricted to the heart muscle, in the case of enteroviral myocarditis and dilated cardiomyopathy.



    Terminology

    Note that when reading the studies, the adenine nucleotide translocator (ANT) has many synonyms, including: adenine nucleotide translocase, translocator protein, ATP/ADP translocator, ADP/ATP translocator, ATP/ADP translocase, and ATP/ADP carrier.

    Even Wikipedia is confused about these synonyms, as there appears to be two Wikipedia articles on the same subject under different synonyms: Adenine nucleotide translocator and ADP/ATP translocase.



    References

    [1] Significance of the adenine nucleotide translocator in the pathogenesis of viral heart disease.
    Schultheiss HP, Schulze K, Dörner A. Mol Cell Biochem. 1996 Oct-Nov;163-164:319-27.
    Full paper here.

    [2] The role of the ADP/ATP carrier in the pathogenesis of viral heart disease.
    Schulze K, Schultheiss HP. Eur Heart J. 1995 Dec;16 Suppl O:64-7.
    Full paper here.

    [3] Disturbance of the myocardial energy metabolism in dilated cardiomyopathy due to autoimmunological mechanisms.
    Schultheiss HP. Circulation. 1993 May;87(5 Suppl):IV43-8.

    [4] Disturbance of myocardial energy metabolism in experimental virus myocarditis by antibodies against the adenine nucleotide translocator.
    Schulze K, Witzenbichler B, Christmann C, Schultheiss HP. Cardiovasc Res. 1999 Oct;44(1):91-100.
    Full paper here.

    [5] Antibodies to ADP-ATP carrier--an autoantigen in myocarditis and dilated cardiomyopathy--impair cardiac function.
    Schulze K, Becker BF, Schauer R, Schultheiss HP. Circulation. 1990 Mar;81(3):959-69.
    Full paper here.

    [6] The postviral fatigue syndrome--an analysis of the findings in 50 cases.
    Behan PO, Behan WM, Bell EJ. J Infect. 1985 May;10(3):211-22.
    Full paper here.

    [7] Chronic fatigue syndrome and mitochondrial dysfunction.
    Myhill S, Booth NE, McLaren-Howard J. Int J Clin Exp Med. 2009 2(1):1-16.
    Full paper here.

    [8] Antibody-mediated enhancement of calcium permeability in cardiac myocytes.
    Schultheiss HP, Kühl U, Janda I, Melzner B, Ulrich G, Morad M. J Exp Med. 1988 Dec 1;168(6):2105-19.
    Full paper here.

    [9] Impaired calcium mobilization in natural killer cells from chronic fatigue syndrome/myalgic encephalomyelitis patients is associated with transient receptor potential melastatin 3 ion channels.
    Nguyen T, Johnston S, Clarke L, Smith P, Staines D, Marshall-Gradisnik S. Clin Exp Immunol. 2017 Feb;187(2):284-293.
    Full paper here.

    [10] Neutralization of IL-17 inhibits the production of anti-ANT autoantibodies in CVB3-induced acute viral myocarditis.
    Yuan J, Yu M, Lin QW, Cao AL, Yu X, Dong JH, Wang JP, Zhang JH, Wang M, Guo HP, Liao YH. Int Immunopharmacol. 2010 Mar;10(3):272-6.
    Full paper here.

    [11] N-acetylglucosamine inhibits T-helper 1 (Th1)/T-helper 17 (Th17) cell responses and treats experimental autoimmune encephalomyelitis.
    Grigorian A, Araujo L, Naidu NN, Place DJ, Choudhury B, Demetriou M. J Biol Chem. 2011 Nov 18;286(46):40133-41.
    Full paper here.

    [12] Adenine nucleotide translocase 1 expression affects enterovirus infection in human and murine hearts.
    Kühl U, Ebermann L, Lassner D, Klingel K, Klumpe I, Winter J, Zeichhardt H, Schultheiss HP, Dörner A. Int J Cardiol. 2014 Apr 1;172(3):e449-52.
    Full paper here.

    [13] The antigenic characteristics and the significance of the adenine nucleotide translocator as a major autoantigen to antimitochondrial antibodies in dilated cardiomyopathy.
    Schultheiss HP, Schwimmbeck P, Bolte HD, Klingenberg M. Adv Myocardiol. 1985;6:311-27.
     
    Last edited: Aug 8, 2017
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  2. Jesse2233

    Jesse2233 Senior Member

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    This is a fascinating theory, great work Hip

    Some questions...

    Would this also disrupt function within the Kreb cycle?

    Under the above model ATP are being produced just not transported, but in Davis' it seems key enzymes needed to carry out glycolysis are shut down. Could the ANT autoantibodies also be disrupting those enzymes?

    I had the same question reading this as well. Perhaps what differentiates ME/CFS from isolated myocarditis is that for whatever reasons the ANT autoantibodies are more widespread thus causing the common systemic derangements.

    However Paul Cheney's research on cardiac abnormalities could indicate a central role for heart dysfunction

    Are there any commercial labs that test for ANT autoantibodies?

    I'd love to know Davis, MyHill, Flue/Mella, and Chia's thoughts on this
     
    Last edited: May 2, 2017
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  3. Jesse2233

    Jesse2233 Senior Member

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    Might this apply to other Enteroviruses such as Coxsackie B4?
     
  4. Jesse2233

    Jesse2233 Senior Member

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    Another question, if a chronic Enterovirus infection is still in place once the B-cells are eliminated, isn't that a recipe for disaster in terms of that infecfion's proliferation? Or would T-cells guard against this?

    Also what about ME/CFS patients without any signs of enterovirus infection?
     
    Last edited: May 2, 2017
  5. kangaSue

    kangaSue Senior Member

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  6. Hip

    Hip Senior Member

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    I wouldn't have thought a blocked mitochondrial ANT protein would directly affect the Kreb's cycle and oxidative phosphorylation in the mitochondria. However, because a blocked ANT protein means the ATP generated in the mitochondria cannot be efficiently transported into the cell, and also means that ADP (= the spent ATP) in the cell cannot be efficiently transported back into the mitochondria for recycling by oxidative phosphorylation, there conceivably could be knock-on effects that cause a slow-down in oxidative phosphorylation. In other words, conceivably oxidative phosphorylation might be automatically down-regulated when there is too much ATP build-up in the mitochondria. That's just my guess.

    The other possibility is that that oxidative phosphorylation might be rendered dysfunctional by a different factor to the one that renders ANT protein dysfunctional.

    Myhill, Booth and McLaren-Howard (MBM) found that the ANT protein was dysfunctional in ME/CFS, and also found oxidative phosphorylation was dysfunctional. They found some ME/CFS patients have an ANT protein dysfunction, other patients have an oxidative phosphorylation dysfunction, and some patients have both. The thread detailing the Myhill, Booth and McLaren-Howard energy metabolism studies is here.


    Fluge and Mella's ME/CFS study suggests a functional impairment in the mitochondrial enzyme pyruvate dehydrogenase, which would imply a reduced ability of mitochondria to take up and utilize the pyruvate created in glycolysis (because pyruvate dehydrogenase is needed to process pyruvate in the mitochondria).

    I wondered whether this inhibition of pyruvate dehydrogenase might actually be a knock-on effect resulting from a blocked ANT protein, and argued for this possibility in this post.

    My idea was that a blockage in ANT protein may lead to a build-up of ATP in the mitochondria (because ANT protein carries the ATP out of the mitochondria and into the cell). This ATP build-up in turn might force the mitochondria to down-regulate pyruvate dehydrogenase, simply because if you can't efficiently transport the ATP out of the mitochondria, it's no good processing more pyruvate to make even more ATP. So that was one possible interpretation of Fluge and Mella's finding that occurred to me.

    However, @Snow Leopard argued quite convincingly against my interpretation in this post.


    Regarding Prof Ron Davis's idea that there may be an issue with glycolysis and the pyruvate kinase enzyme (this enzyme is the final step of glycolysis which manufactures pyruvate): as yet we don't have much published details about this pyruvate kinase impairment he has found, so without these details, it is hard to analyze how this might fit in with the blocked ANT protein theory of ME/CFS.



    A few months ago I wrote to Dr John McLaren-Howard, who runs Acumen Lab which performs the mitochondrial testing used by Dr Myhill, asking whether the blockages his lab finds on the ANT protein could be due to an ANT autoantibody.

    Dr McLaren-Howard very kindly replied to my email: he said that in around 40% of ME/CFS patients whose blood is analyzed by his lab, a significant of blocking of ANT protein functioning is found. However, he said that when his lab investigates this blocking further, they find "chemical causes for the blocking in around 75% of that group" — I presume by that he means the ANT protein appears to be clogged up by exogenous environmental chemicals. And he said that only a small number of patients have immunoglobulins on their mitochondrial membranes (an autoantibody is an immunoglobulin). So at least via the methods he uses in his lab, there does not seem to be a great deal of evidence for an ANT autoantibody in ME/CFS.



    I should think so. VP proteins are found on the protein shell (capsid) of a viral particle (VP protein = viral particle protein). Here is a diagram of the four types of VP protein (VP1, VP2, VP3 and VP4) found on enterovirus shells:

    The Four VP Capsid Proteins of Enterovirus
    Picornaviridae_virion.jpg
    Source: here.​

    I believe the enterovirus VP capsid proteins are quite conserved among different enteroviruses, so the ANT autoantibody that the German myocarditis researchers suggest is triggered by molecular mimicry to enterovirus VP proteins should be triggerable by all enteroviruses.

    However, not all enteroviruses hang around in the body as long term persistent intracellular infections. To my knowledge, coxsackievirus B and echovirus are the only enteroviruses that can form these persistent intracellular infections, and these happen to be the enteroviruses linked to ME/CFS. Other enteroviruses such as rhinovirus (a common cold virus) are quickly cleared from the body by the immune system, so I guess they would probably not have the opportunity to trigger autoimmunity and trigger an ANT autoantibody.

    If you subscribe to this theory of autoantibodies being triggered by molecular mimicry to proteins found on infectious pathogens (and Jonathan Edwards is certainly not a fan of such theories), then in order for the pathogen to be constantly driving the production of autoantibodies, I would think that this pathogen needs to be able to form a persistent long term infection in the body.

    Note that VP capsid proteins are not unique to enteroviruses: they are found in the shells of other viruses too. But as far as I am aware, these VP proteins will be genetically different in different viral families.

    I wonder though if all the viruses which are linked to triggering ME/CFS might have VP proteins that molecularly mimic the ANT protein. Viruses and other pathogens whose proteins are molecular mimics of the ANT protein might thereby have a propensity to triggering ME/CFS.



    I wouldn't think so, because I understand from @Jonathan Edwards that when rituximab kills off the B-cells, after some months, the plasma cells that manufacture autoantibodies seem to die off (and are not replaced, because the B-cells they derive from have all been killed); however, the plasma cells that manufacture the regular antibodies that target infectious pathogens in the body do not die off, and so they continue to provide immune protection against these pathogens. Which is a rather handy state of affairs, otherwise it would be doubtful if you could ever use rituximab safely, if it also led to the loss of antibodies as well as autoantibodies.

    The likely reason for this selective die off of the autoantibody-producing plasma cells only is that autoantibodies are probably generally manufactured by short lived plasma cells, whereas most of the antibodies that target pathogens in the body are likely generally manufactured by long lived plasma cells. Jonathan Edwards explains it in this post.



    I can think of several possibilities that might explain non-enterovirus ME/CFS. The first possibility is that ME/CFS associated with other viruses, such as Epstein-Barr virus, might be due to a different mechanism entirely.

    A second possibility might be that a latent pre-existing infection with enterovirus is already present in the body, but it has not triggered any autoimmunity or autoantibodies; but then when that person later catches EBV or some other ME/CFS-linked virus (or is given an ME/CFS-linked vaccine such as the hep B vaccine), that virus or vaccine alters the immune landscape, and somehow facilities the triggering of ANT autoantibodies by the latent enterovirus infection (OK, I am clutching at straws here).

    A third possibility is the idea I mentioned above, which is that all the all the viruses linked to ME/CFS might have VP proteins that molecularly mimic the ANT protein, and so all these viruses may trigger ME/CFS by the same mechanism — by the fact that their VP protein mimics ANT protein, and thus has a propensity to triggering an ANT autoantibody.

    It would be interesting to look at the genetic structure of the VP proteins of all the viruses linked to ME/CFS, to see if the same peptide sequence found in the enterovirus VP protein is also present in these other ME/CFS-linked viruses (I mean the enterovirus VP protein peptide sequence that the German myocarditis researchers said is molecularly similar to the ANT protein). It could simply be that ME/CFS can be triggered by any persistent pathogen whose proteins are molecularly similar to the ANT protein.

    The viruses most linked to triggering ME/CFS are: coxsackievirus B, echovirus, Epstein-Barr virus, parvovirus B19, cytomegalovirus and HHV-6.
     
    Last edited: Aug 6, 2017
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  7. Hip

    Hip Senior Member

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    I should mention that I did try to contact by email the two main German researchers who have studied the ANT autoantibody from the early 1980s onwards: Prof Heinz-Peter Schultheiss (he works at Charité, Berlin) and Dr Karsten Schulze.

    I asked them whether they think the chronic coxsackievirus B (CVB) infections that studies show many ME/CFS patients have in their skeletal muscles might be inducing ANT autoantibodies in those muscles, and whether these ANT autoantibodies might explain the low energy state and energy metabolism dysfunctions of ME/CFS.

    If CVB infections of the heart muscle can trigger these ANT autoantibodies, why not CVB infections of the skeletal muscles? (Although cardiac muscle is different to skeletal muscle).

    Unfortunately they have not answered my emails (which were in English but also translated into German).
     
  8. flitza

    flitza Senior Member

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    Fantastic post, Hip! Thank you.
     
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  9. Hip

    Hip Senior Member

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    Thank you flitza, glad you found it of interest. (You might want to edit your above post to remove that very large quote, as it makes thread look a bit messy and confusing).
     
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  10. flitza

    flitza Senior Member

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    I'll work on it. Not so good with that stuff, editing...
     
  11. Jesse2233

    Jesse2233 Senior Member

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    @Hip any conceivable way Naviaux's cell danger response, and anti-purinergic therapy could fit into this model?
     
  12. Hip

    Hip Senior Member

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    I'd would tend to view Naviaux's idea of a cell danger response closing down metabolism as a different and competing theory to Behan's anti-mitochondrial autoantibody theory.

    An anti-mitochondrial autoantibody theory I think could easily fit into, and possibly explain, the Myhill, Fluge & Mella, and Ron Davis theories of ME/CFS metabolic dysfunction. But the Naviaux cell danger response model of ME/CFS is, if I understand it correctly, is based on a fundamentally different model of immunity: the danger model.

    The regular self / non-self model of immunity proposes that the immune system responds and attacks anything that is foreign to the body. By contrast, the danger model of immunity proposes that the immune system responds to anything that is a danger to the body. I have not spent any time reading about the danger model, and I think that would be a prerequisite in order to properly get to grips with the Naviaux perspective on ME/CFS.
     
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  13. Jesse2233

    Jesse2233 Senior Member

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    Setting aside the larger philosophical questions of the CDR, might blocking the purinergic signaling system with a drug such as Suramin fit within the context of Behan's model?
     
  14. Hip

    Hip Senior Member

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    From my very limited understanding of Naviaux's work, I cannot see any connection between Naviaux's ideas and Behan's anti-mitochondrial autoantibody hypothesis. They are chalk and cheese.
     
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  15. Jesse2233

    Jesse2233 Senior Member

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    Perhaps Secukinumab could be a treatment method. It's an FDA approved monoclonal antibody that targets IL-17, and has also shown to be protective against autism in mice
     
    Last edited: Jun 16, 2017
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  16. wastwater

    wastwater Senior Member

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    I find this mention of Th-17 interesting as I likely have a deletion at FOXC1(6p25.3)affecting IRF4
    Once you pop you can't stop I was thinkin, EBV in my case and measles
     
    Last edited: Jul 7, 2017
  17. Jesse2233

    Jesse2233 Senior Member

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    Perhaps it would be worthwhile to contact Carmen Scheibenbogen and Oystein Fluge with this information as well
     
  18. Hip

    Hip Senior Member

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    I already emailed Fluge and Mella, but unfortunately they did not reply, so I am not sure if they found ANT autoantibodies of interest or not. I believe Carmen Scheibenbogen's main focus is EBV-associated ME/CFS, so enterovirus etiologies may not be her thing. But I will send her a quick email anyway.
     
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  19. Jesse2233

    Jesse2233 Senior Member

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    Thanks Hip. Mark Davis might be another prospect
     
  20. drob31

    drob31 Senior Member

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    Keep sending emails.
     
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