Abstract
THE immunopathological basis of the acutely fatal convulsive central nervous system (CNS) disease produced in adult mice following cerebral infection with lymphocytic Choriomeningitis (LCM) virus is well established1. Thus, a variety of immuno-suppressive treatments, given to adult mice inoculated intracerebrally with a potentially lethal dose of virus, produce a transient or permanent ablation of both the histological and clinical correlates of LCM. Permanently protected mice usually maintain high virus concentrations in their brains and blood for life2,3, presenting a picture which, on virological grounds, is strikingly similar to the lifelong virus carrier state arising in mice inoculated with LCM virus shortly after birth3,4.
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