EBV and Autoimmunity…Is there anything special about MS?


We have all heard the view that EBV is part of the cause and MS, but one can argue, indeed I have, that there is nothing special about MS. EBV does not simply just cause MS, it is part of the cause of autoimmuity of a number of conditions. If true then simply targeting MS may not be the best way of showing this. So what is the proof that EBV just causes MS?

We all know some stuff…..but it is circumstantial. Sure I accept that you have to get infected to get MS….but they didn’t look to show that getting infected did not cause an ingrowing toenail or rheumatoid arthritis, Lupus of Sjogren’s syndrome for that matter.

But we know that getting glandular fever increases you risk of geting MS…but it is not just MS it is a host of other conditions, here it is an intestinal inflammatory disease.

So it is easier to show that EBV is not just associated with EBV and the idea that EBV is just the cause of MS is a bit weaker. So how you deal with it, is a bit more complex and asks if MS is the best place to test this idea? Other coniditions have alot more people, some have alot less treatments available

Infectious mononucleosis is associated with an increased incidence of Crohn’s disease: results from a cohort study of 31 862 outpatients in Germany. Loosen SH, Kostev K, Schöler D, Orth HM, Freise NF, Jensen BO, May P, Bode JG, Roderburg C, Luedde T.Eur J Gastroenterol Hepatol. 2023 Mar 1;35(3):255-260.

Conclusion: Infectious mononucleosis is significantly associated with an increased incidence of Crohn’s disease but not ulcerative colitis, especially in young female patients. Our data support the hypothesis of a pathophysiological involvement of EBV in the development of Crohn’s disease and should trigger molecular research to further dissect the pathophysiology of IBD.

So the point is we have seen MS therapies being developed to target EBV……however, is it too late to do it after you have MS? Also what is the control group for the trials? 

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  • .but they didn’t look to show that getting infected did not cause an ingrowing toenail or rheumatoid arthritis, Lupus of Sjogren’s syndrome for that matter.

    Like that bit

    P,G says that pwms have ebv in the brain?

    Do you agree?

    anti-EBV T-cell responses are increased in people on natalizumab, despite natalizumab being an effective DMT, suggests the CNS compartment is where the action is (EBV replication)

    Also people with Ra have Ebv in the joints ,Lupus patients have Ebv in the heart,kidney,Liver,sytemic sclerosis patients have ebv in the in the skin?


    • PG says pwms have EBV in the brain….maybe but plenty have people have looked and haven’t found it….are they looking hard enough?

      EBV increased with T cell responses, surely if stuff is trapped in blood all viral responses in blood are increased.
      Glofitamab…a CD20, CD3 multispecific antibody that is silenced to not deplete directly. What is the advantage over anti CD20 it is even less likely to get into brain it doesnt deplete via the usual mechanisms and so won’t protect itslef as much ADA here we do a new glow for a new glo.

      • So PG is making statements that he cannot prove?

        Hes probably gonna turn around and say hey B cells is in pwMS’s brain and thats ur EBV.

        If EBV is in the brain also what other cells could it infect?

        • You never prove you disprove….Popper theory

          Turn round…yep

          EBV infects B cells via certain receptors it also infect epithelial cells but if this is the reason why is MS a disease of the brain, those B cells are going to be all over the body.

          • Yes, and here is a frustrating problem. There is now an extensive list of inflammatory conditions, some “autoimmune'(with definite antigenic targets) and some not obviously autoimmune, and some not autoimmune, in which EBV has been detected and suggested to be a putative ’cause’. But where ever B cells are found in the above there will inevitably be latent or activated EBV, and HHV6 will turn up for the same reason as it is latent in T cells. Passengers? Contributors? necessary causes? A nice headache!

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