EBV B cells make mice worse


This is ProfG’s turf, but MD2 pointed this one out and said what do you make of it?…I dont’t its profGs turf

You have every thing here…EBV, microbiota, relapse what more do you want?…Replication I guess

Epstein Barr virus-immortalized B lymphocytes exacerbate experimental autoimmune encephalomyelitis in xenograft mice.Polepole P, Bartenslager A, Liu Y, Petro TM, Fernando S, Zhang L.J Med Virol. 2020. doi: 10.1002/jmv.26188.

Multiple sclerosis (MS) is the most common autoimmune disorder affecting the central nervous system. Epstein-Barr virus (EBV) is a causative agent for infectious mononucleosis (IM) that is associated with MS pathogenesis. However, the exact mechanism by which EBV, specifically in IM, increases the risk for MS remains unknown. EBV immortalizes primary B lymphocytes in vitro and causes excessive B lymphocyte proliferation in IM in vivo. In asymptomatic carriers, EBV-infected B lymphocytes still proliferate to certain degrees, the process of which is tightly controlled by the host immune systems. Experimental autoimmune encephalomyelitis (EAE) mimics key features of MS in humans and is a well-established rodent model for human MS. We have found that xenografts of EBV-immortalized B lymphocytes, which partially resemble the hyperproliferation of EBV-infected cells in IM, exacerbate autoimmune responses in myelin oligodendrocyte glycoprotein-induced EAE in C57BL/6 mice. After remission, an additional challenge with EBV-immortalized cells induces a relapse in EAE. Moreover, xenografts with EBV-immortalized cells tighten the integrity of blood brain barrier (BBB) in thalamus and hypothalamus areas of the mouse brains. Genomic sequences of prokaryotic 16S rRNA presented in faeces reveal that EBV-immortalized cells significantly change the diversities of microbial populations. Our data collectively suggest that EBV-mediated proliferation of B lymphocytes may be a risk factor for the exacerbation of MS, which are associated with gut microbiome changes and BBB modulations. Furthermore, multiple xenografts of EBV-immortalized cells into in C57BL/6 mice could sevre as a useful model for human relapsing-remitting MS with predictable severity and timing.

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  • Excellent 👍🏼 I barely understood what you are studying but feel you’re getting closer to what we MS patients long for: Understanding and Cure. I keep thinking about lymph nodes and mononucleosis and the other physiological changes I went through with a bad case living in a dormitory half dead. I thought the Severity was bad. They gave me a steroid taper starting at 80 mg to none in 8 days. I never slept but really couldn’t do a thing. I think asking MS-ers about their Mono history with details would be interesting compared to non mono people. I still think “yuk” remains after virus dies, leaving carcasses 🦠 stuck in the lymphatic system scraping at the BBB, clawing, abrading. Too big to pass. Not water soluble. If I’m so off base you can say so. But day after day I ponder what this MonSter is doing and how can I make it go away?

  • If I remember it right, the memory cells remember bad things in a 2-step-process. 1)Check if it recognizes something foreign and step 2) Check if it does not recognize something of the own body.
    If step 2 fails, self destruction gets initialized.

    Maybe here comes EBV into play. Maybe sometimes, the memory cells get infected before step 2 and then the self destruction fails. This would leave a memory cell with wrong memory in the body.

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