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A pipeline was developed to quantify EBV DNA from whole-genome sequencing data in a cohort of over half million subjects identifying 39 susceptibility risk loci. A significant overlap with genetic variants associated with MS risk was observed p<10-12. These data suggest that EBV-infected B cells may constituted a critical hub that modulates T cell responses while activating MS gene linked susceptibility pathways within B cells. Finally, B cell depletion is almost totally effective in stopping autoimmune MS. Thus, we define a genetic and cellular framework linking B cells to the initiation of MS and support a causal role of EBV activity on MS risk.
