Epstein-Barr virus in multiple sclerosis.
Recent seroepidemiologic and pathologic evidence suggests that prior infection with Epstein-Barr virus (EBV) may be necessary for the development of multiple sclerosis (MS). EBV infects more than 90% of all humans, most of whom remain healthy. In contrast, 99% of MS patients have evidence of prior infection with EBV. EBV infects resting B lymphocytes, immortalizing them into long-lived memory B cells that survive largely undetected by the immune system in the peripheral circulation. MS patients show elevated titers to EBV years before developing any neurologic symptoms. Postmortem pathologic analysis of brains of patients with MS has revealed diffuse EBV-associated B-cell dysregulation in all forms of MS. Theories of pathogenesis of EBV in MS include antigenic mimicry, immortalization of B-cell clones, and cytotoxic T-cell dysfunction against virally infected B cells. This article reviews the existing evidence of the relationship between EBV and MS and considers the therapeutic implication of this evidence.
Bagert
Bridget A
BA
Department of Neurology, 1542 Tulane Avenue, Room 718B, Louisiana State University Health Science Center, New Orleans, LA 70112, USA. bbager@lsuhsc.edu
D000914:Antibodies, Viral / Q000276:immunology; D000956:Antigens, Viral / Q000276:immunology; D001921:Brain / Q000276:immunology / Q000473:pathology / Q000821:virology; D020031:Epstein-Barr Virus Infections / Q000150:complications* / Q000276:immunology / Q000473:pathology / Q000821:virology; D004854:Herpesvirus 4, Human / Q000276:immunology / Q000502:physiology; D006801:Humans; D007070:Immunoglobulin A / Q000276:immunology; D007074:Immunoglobulin G / Q000276:immunology; D009103:Multiple Sclerosis / Q000209:etiology* / Q000276:immunology / Q000473:pathology / Q000821:virology; D012307:Risk Factors; D017735:Virus Latency
D000914:Antibodies, Viral; D000956:Antigens, Viral; D007070:Immunoglobulin A; D007074:Immunoglobulin G