FURTHER ULTRASTRUCTURAL OBSERVATIONS OF VIRUS MORPHOGENESIS AND MYELIN PATHOLOGY IN JHM VIRUS ENCEPHALOMYELITIS

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Abstract
Fleury H.J.A., Sheppard R.D., Bornstein M.B. & Raine C.S. 1980 Neuropathology and Applied Neurobiology 6,165–179Further ultrastructural observations of virus morphogenesis and myelin pathology in JHM virus encephalomyelitisGroups of 3, 17, and 28‐day‐old Swiss mice were inoculated intracerebrally with JHM virus, the neurotropic strain of mouse hepatitis virus (MHV), and studied serially by virologic and morphologic techniques. Beginning 2–5 days post‐inoculation, all groups of infected mice developed CNS lesions which were destructive in the 3‐day‐old group and demyelinative in the 17 and 28‐day‐old animals. Infectious virus could be isolated from the brain, spinal cord, and liver. Electron microscopy demonstrated the virus to be pantropic in the CNS with virions occurring within ependymal cells, astrocytes, neurons, oligodendrocytes, endothelial cells, and cell of haematogenous origin. Giant cell formation was a constant feature. In regions of demyelination, oligodendrocytes exhibited a propensity to proliferative aberrant membrane. Myelin degradation was accompanied by membrane vesiculation and by the stripping action of macrophages. The lesions were not due to CNS elements in the inoculum since in animals inoculated with normal CNS suspensions from appropriate age groups failed to show lesions. The morphogenesis of JHM virions was followed ultrastructurally as was the formation of syncytia in the different cell types. In addition to delineating virus morphogenesis and myelin pathology, the results underscore the pantropic nature of JHM virus in the CNS, the systemic nature of the infection, and that oligodendrocytes were the principal targets.