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Genetic and environmental factors determine the susceptibility to develop multiple sclerosis (MS). Improved epidemiologic study designs helped identify environmental risk associations for MS, such as a history of infectious mononucleosis (IM), a symptomatic primary infection with the human γ-herpesvirus Epstein-Barr virus (EBV). EBV preferentially infects B lymphocytes and persists lifelong in a transcriptionally quiescent state in circulating latently infected memory B cells (0.5 to 50 per million). Lytic EBV infection can occur from the memory B-cell pool, presumably after an encounter with the cognate B-cell receptor antigen. The immune control of EBV infection centers around strong memory CD4+ and CD8+ T-cell responses, whereby the CD4+ T cells maintain EBV-specific immunity, and both CD4+ and CD8+ T cells can target EBV-infected cells directly.
Patients with MS are nearly universally seropositive for EBV (i.e., close to 100% in adults and >90% in children) compared with seropositivity rates of 90%–95% in adults and less than 80% in age-matched pediatric cohorts and show deregulated T-cell and antibody responses to EBV-encoded antigens. These changes are initiated early in disease development, since increased EBV-specific antibody titers are detectable as early as 5 or more years before the clinical onset of MS.1 In patients with clinically isolated syndromes and …
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