Abstract
Recent evidence suggests that infection with the Epstein Barr virus (EBV) initiates a prodromal phase of multiple sclerosis (MS) in individuals with genetic and environmental predispositions for this autoimmune disease. In the context of the main genetic risk factor, the major histocompatibility complex (MHC) class II molecule HLA-DRB1*1501, EBV infection is less well controlled in a preclinical mouse model. CD4+ T cells that are primed during EBV infection and recognize EBV transformed B cells in an HLA-DRB1*1501 restricted fashion, cross-react more frequently with myelin autoantigens that are thought to mediate MS. While EBV emerges as an important, possibly essential trigger of MS, more mechanistic insights into this connection are required to understand if targeting of EBV infection itself or of cross-reactive immune responses that recognize both viral and autoantigens might prevent or even allow to treat MS.
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