Abstract
Multiple sclerosis (MS), one of the most common neurological diseases of young adults, is accompanied by inflammatory demyelination and loss of oligodendrocytes in the central nervous system (CNS). Although its etiology remains unclear, a generally accepted hypothesis is that virus infections could initiate a CNS-directed immune process in a genetically predisposed host (Oldstone 1997). Amongst various animal models of virus-induced demyelination, studies on murine hepatitis virus (MHV) have revealed that this virus is capable of causing direct oligodendrocyte cytopathology, but may also elicit a variety of immunopathological responses (Lane and Buchmeier 1997). Given that MHV causes MS-like CNS demyelination, the related human coronaviruses (HCoV) represent a logical target of investigation as a potential microbial agent involved in MS pathogenesis.
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