Viruses can silently prime for and trigger central nervous system autoimmune disease

Although many viruses have been isolated from patients with multiple sclero sis (MS), as yet, no one agent has been demonstrated to cause MS. In contra st, epidemiological data indicate that viral infections are associated with exacerbations of MS. Here, we present data showing that virus infections c an subclinically prime animals for central nervous system (CNS) autoimmune disease; long after the original infection has been eradicated, a nonspecif ic challenge/infection can trigger an exacerbation. The priming infectious agent must show molecular mimicry with self-CNS antigens such as glial fibr illary acidic protein (GFAP), myelin associated glycoprotein (MAG) or myeli n proteolipid protein (PLP). The subsequent challenge, however, may be nons pecific; complete Freund's adjuvant (CFA), or infection with a recombinant vaccinia virus encoding an irrelevant protein, could trigger CNS disease. I n the CNS, we could detect a mononuclear cell infiltration, but no demyelin ation was found. However, if the pathogenesis of MS is similar to that of t his novel animal model for CNS autoimmune disease, our findings could help explain why exacerbations of MS are often associated with a variety of diff erent viral infections.