Mouse hepatitis virus (MHV) A59 infection which causes acute encephalitis, hepatitis, and chronic demyelination, is one of the experimental models for multiple sclerosis. Previous studies showed that lethal infection of β2-microglobulin ‘knockout’ (β2M(–/–)) mice required 500-fold less virus and viral clearance was delayed as compared to infection of immunocompetent C57Bl/6 (B6) mice. To investigate the mechanism of the increased susceptibility of β2M(–/–) mice to MHV-A59, we studied organ pathology and the distribution of viral antigen and RNA during acute and chronic infection. A59-infected β2M(–/–) mice were more susceptible to acute encephalitis and hepatitis, but did not have increased susceptibility to demyelination. Viral antigen and RNA distribution in the brain was increased in microglia, lymphocytes, and small vessel endothelial cells while the distribution in neurons and glia was similar in β2M(–/–) mice and B6 mice. Acute hepatitis and thymus cortical hypoplasia in β2M(–/–) mice were delayed in onset but pathologic changes in these organs were similar to those in B6 mice. The low rate of demyelination in β2M(–/–) mice was consistent with the low dose of the virus given. A less neurotropic virus MHV-2, caused increased parenchymal inflammation in β2M(–/–) mice, but without demyelination. Thus, CD8+ cells were important for viral clearance from endothelial cells, microglia and inflammatory cells, but not from neuronal and glial cells. In addition, CD8+ cells played a role in preventing the spread of encephalitis.

Keywords:
Coronaviruses, Nidoviruses, Immunohistochemistry, In situ hybridization, Pathogenesis
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1999
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