Neuroinflammation as a result of non-neurotropic herpesvirus infection.

The non-neurotropic Epstein Barr virus (EBV) has been suggested to initiate the prodromal phase of multiple sclerosis (MS), often years before the first clinical symptoms. This review discusses mechanisms by which EBV might cause neuroinflammatory B-cell migration to the central nervous system (CNS), as observed during primary CNS lymphomas and MS. Furthermore, mechanisms of molecular mimicry and autoreactive B-cell expansion by EBV will also be summarized. Finally, approaches to target EBV-mediated neuroinflammation for therapeutic interventions in people with MS (pwMS) will be explored. The recently provided information on EBV's association with MS gives exciting insights into the initiation of this autoimmune disease. Successful therapeutic interventions on the basis of this knowledge might provide evidence that EBV contributes also to the clinical phase of this autoimmune disease.