中国科学技术大学领衔，三篇Cell论文揭示EB病毒感染导致多发性硬化症发生的新机制

Core Viewpoint - The article discusses the relationship between Epstein-Barr virus (EBV) infection and the development of Multiple Sclerosis (MS), highlighting new research that connects environmental and genetic risk factors in MS pathogenesis [3][4][9]. Group 1: Research Findings - A study published in the journal Cell reveals that EBV infection and the HLA-DR15 gene jointly drive the development of MS by presenting myelin peptide antigens and activating autoreactive CD4+ T cells [4][11]. - The research indicates that EBV infection alters the transcriptional and immunopeptidomic profiles of B cells, particularly in individuals carrying the high-risk HLA-DR15 genotype, leading to the presentation of specific myelin basic protein (MBP) peptides [8][9]. - The study provides direct evidence supporting the "molecular mimicry" hypothesis, where similarities between EBV proteins and myelin proteins lead to an autoimmune response against the nervous system [9][18]. Group 2: Implications for Treatment - The findings deepen the understanding of MS etiology and suggest potential new therapeutic approaches targeting specific autoreactive T cells or EBV-infected B cells [11][18]. - The research collectively illustrates how EBV infection can influence both B cell function and induce cross-reactive T cell responses, contributing to MS pathogenesis [18].