INTERPLAY BETWEEN VIRUSES AND B CELLS IN THE PATHOGENESIS OF MULTIPLE SCLEROSIS.

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Multiple sclerosis (MS) is a chronic progressive autoimmune neurological disease and themost common demyelinating disorder in Western countries. Although significant progresshas been made in providing new therapeutic strategies, identification of definitive triggersfor MS has proven elusive. Many factors are known to be involved, including UVB levels andvitamin-D and Human endogenous retrovirus (HERV). However, recent studies have shownEpstein-Barr Virus (EBV) is the single biggest risk factor for MS Importantly, theircontribution to the pathogenesis of MS remains unknown.In this project we aim to understand how EBV, B cell differentiation status and innateimmunity co-operate to trigger reactivation of HERV-W in B cells. Thereafter, using B cellsfrom the cerebrospinal fluid of MS patients, we will explore how these factors co-operateto generate cross-reactive antibodies targeting both viral proteins and MS autoimmunetargets, including myelin. By pinning down how the viruses contribute tothe pathogenesis of MS, we will open-up badly needed new treatment andprevention avenues for the disease, principally aimed at controlling the triggering causesrather than just modifying the later immune damage.