The growth of four human and animal enteroviruses in the central nervous systems of mice.

The pattern of CNS infection of our enteroviruses, Coxsackievirus A14, encephalomyocarditis (EMC) virus, GDVII virus, and Vilyuisk virus, was investigated. The regional sites of virus replication were correlated with pathological changes. These viruses were found to replicate and produce similar lesions in selected sites in the mouse CNS during acute infection. Virus antigen and histological lesions were essentially confined to the gray matter, with additional but less direct support for this being provided by virus assay of CNS regions. Virus antigen only could be confidently identified in neurons, and, histologically, neurons were observed in various stages of degeneration. The distribution of the involvement varied in the different infections. For example, EMC virus infection primarily affected the cerebral hemispheres and thalamus, while Coxsackievirus a14 infection predominantly involved the brainstem and spinal cord. GDVII and Vilyuisk virus infections more uniformly involved the entire neuraxis. There was no evidence of virus replication in the olfactory bulbs, leptomeninges, ependyma, choroid plexus, and vascular endothelium. The cerebellum was generally spared, with the cerebellar hemispheres affected only in Coxsackievirus A14 infection. It therefore appears that enteroviruses selectively infect different populations of nerve cells.