Parainfluenza virus Sendai infection in macrophages, ependyma, choroid plexus, vascular endothelium and respiratory tract of mice.

Immunofluorescent observations showed that after intranasal instillation of parainfluenza 1 (Sendai) virus into adult mice, infection is confined to the epithelial lining of the larger airways. Alveolar macrophages were not significantly involved, although they could be infected in vitro. In suckling mice, the infection was more acutely lethal and extended into the terminal air spaces. The intranasal susceptibility of adult mice was not reproducibly affected by treatment with potent antithymocyte serum, and there were no obvious pathogenic effects when heterologous antiserum was instilled intranasally into infected mice. Peritoneal macrophages were infected by intraperitoneally injected Sendai virus, with production of a highly viscous peritoneal exudate. Kupffer cells of the liver and endothelial cells in large veins and auricles were infected by intravenously injected virus. When injected intracerebrally, Sendai virus infected ependyma and choroid plexus epithelium. Adult mice often survived, in spite of ependymal destruction and changes in ventricular morphology. Astrocytes were activated but not infected.