Abstract
Mouse hepatitis virus, type-4 (strain JHM) has been studied extensively as a model for neurologic disease. Intracerebral infection may lead to fatal encephalomyelitis or may be limited to demyelination (1). Prior to demyelination by myelin stripping macrophages (2), connections between myelin-forming oligodendrocytes and myelin sheaths, not ordinarily visible in the adult nervous system, become apparent (3). Of particular interest, in regard to this observation, demyelination in this model system is followed by remyelination mediated by oligo-dendrocytes (4, 5). However, virus persistence and limited areas of recurrent demyelination may occur (5, 6).
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