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Although the causes of Multiple Sclerosis (MS) still remain largely unknown, multiple lines of evidence suggest that <i>Epstein–Barr virus</i> (EBV) infection may contribute to the development of MS. Here, we aimed to identify the potential contribution of EBV-encoded and host cellular miRNAs to MS pathogenesis. We identified differentially expressed host miRNAs in EBV infected B cells (LCLs) and putative host/EBV miRNA interactions with MS risk loci. We estimated the genotype effect of MS risk loci on the identified putative miRNA:mRNA interactions in silico. We found that the protective allele of MS risk SNP rs4808760 reduces the expression of <i>hsa-mir-3188-3p</i>. In addition, our analysis suggests that <i>hsa-let-7b-5p</i> may interact with <i>ZC3HAV1</i> differently in LCLs compared to B cells. In vitro assays indicated that the protective allele of MS risk SNP rs10271373 increases <i>ZC3HAV1</i> expression in LCLs, but not in B cells. The higher expression for the protective allele in LCLs is consistent with increased <i>IFN</i> response via <i>ZC3HAV1</i> and so decreased immune evasion by EBV. Taken together, this provides evidence that EBV infection dysregulates the B cell miRNA machinery, including MS risk miRNAs, which may contribute to MS pathogenesis via interaction with MS risk genes either directly or indirectly.