Microbial infection generates pro-inflammatory autoimmunity against the small heat shock protein alpha B-crystallin and provides the fuel for the development of multiple sclerosis

The idea that microbial infections play a role in the development of multiple sclerosis (MS) is as old as the notion itself that MS represents a distinct neurodegenerative disease. Epidemiological data on MS, the appearance of characteristic oligoclonal populations of IgG in the cerebrospinal fluid, elevated serum Ig levels to several viruses, associations between MS relapses and infections and the frequent presence of viral infections in MS brains are all consistent with the idea that infections, in particular with Epstein-Barr virus (EBV) somehow play a role [1-5]. Also animal models of viral infections in the central nervous system (CNS) confirm the ability of such infections to trigger chronic demyelinating disease. Frustratingly however, EBV and other pathogens so far implicated in the pathogenesis of MS are all rather ubiquitous and so far, they have never been found to be specific for MS. Current data therefore point to a relationship between microbial infection and MS that is more complex than a simple “one agent — one disease” paradigm.