Of note, the shift in the B cell subset distribution associated with HCMV in our untreated MS patients was reminiscent of the impact of IFNβ therapy in HCMV seronegative RRMS patients, an effect that might be hypothetically related with interferon-signaling pathways induced by persistent HCMV infection [20]. Here, IFNB1 is linked to cytomegalovirus infection.