Mechanistic synthesis uncovers an EBV-driven circuit linking genetic risk to central nervous system autoimmunity in multiple sclerosis, highlighting targets for EBV-directed prevention.
Five recent publications establish a “Gate–License–Amplify” circuit that mechanistically links Epstein–Barr virus (EBV) infection and genetic risk (HLA-DR15) to the pathogenesis of multiple sclerosis (MS). 1 , 2 , 3 , 4 , 5 This new model reveals how EBV reprograms immunopeptidomes to trigger CNS autoimmunity, providing a molecular rationale for the efficacy of B-cell depletion and supporting EBV-directed prevention as a realistic goal.
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Li et al. (2026) studied this question.
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