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MS is an idiopathic, chronic inflammatory syndrome of CNS white matter. Cellular and humoral immune elements occur at zones of ongoing white matter destruction, although their prevalence varies.1 In this issue of Neurology, Wandinger et al.2 use sophisticated serologic and genetic methods to study an association between Epstein–Barr virus (EBV) infections and the diagnosis and symptoms of MS. Can common pathogens trigger demyelination? If so, clarifying the etiology (etiologies) of the MS syndrome might lead to specific therapies.
There have been two parallel hypotheses for the pathogenesis of MS: 1) autoimmune, with immune injury to an essentially normal CNS; and 2) infectious, with chronic or reactivated latent infection provoking the immune injury. Recently, these hypotheses have been fused into a third: a common pathogen drives or initiates autoimmunity, whether or not the pathogen resides in the CNS.
Inflammatory diseases resembling MS can be autoimmune or infectious (or parainfectious). There are noninfectious experimental models of acute and chronic CNS demyelination, but these models rely on lymphocytes derived in a milieu similar to infection-powerful adjuvants and brain peptides. However, there are numerous naturally occurring mammalian diseases similar to MS, each caused by an interaction between a neurotropic virus …
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