Epstein–Barr virus infection and the risk of developing multiple sclerosis Review article

Abstract

Despite increasing amounts of data regarding the pathogenesis of multiple sclerosis (MS), its etiology remains unknown. MS is believed to develop by interplay of genetic predispositions and environmental factors, including infectious ones, which disturb proper immune surveillance. More and more data indicate that the infectious agent is the Epstein–Barr virus (EBV). Although infection with it is usually asymptomatic in childhood, the ability of the virus to convert into a latent form with limited gene expression allows it to avoid host immune surveillance. It initiates a cascade of immunological processes leading to severe clinical implications, e.g., in the development of autoimmune diseases. Previous studies have shown that anti-EBV antibodies exist in almost all patients with multiple sclerosis. The most extensive population-based study in recent years covered US Army conscripts and found that the risk of developing multiple sclerosis is 32 times higher after infection with this virus. Determining the exact relationship between the Epstein–Barr virus and multiple sclerosis, including assessing the influence of genetic and environmental factors on this correlation, may be very important for understanding pathogenesis of multiple sclerosis and other autoimmune diseases. Such insights will also enable the identification of targets for future personalized therapies, especially in the context of increasingly widely used B cell depletion therapies.