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Ross river virus‐induced demyelination: I. Pathogenesis and histopathology
Author(s) -
Seay Alan R.,
Wolinsky Jerry S.
Publication year - 1982
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410120411
Subject(s) - pathology , brainstem , pathogenesis , myelin , virus , encephalomyelitis , infiltration (hvac) , mononuclear cell infiltration , histopathology , spinal cord , cerebellum , gliosis , immunosuppression , medicine , biology , immunology , multiple sclerosis , central nervous system , neuroscience , physics , thermodynamics
Abstract Ross River virus (strain T48) infection in mice causes and encephalomyelitis characterized by focal, primary demyelination in the cerebellum, brainstem, and spinal cord. Maximal serum and brain content of virus occurs on days 2 and 4, respectively. Virus is not detectable in serum after day 3 or in brain after day 9. Histopathological lesions are present by day 2 and consist of perivascular macrophage and polymorphonulcear leukocyte infiltration, focal necrosis in the internal granule cell layer, and myelin disruption. Mononuclear cell infiltrates are present by day 5. Foci of demyelination in the presence of preserved axons become more widespred by day 8, and early partial remyeliantion occurs by day 13. Immunosuppression reduces the mononuclear dell infiltration but does not alter the demyelination. Althogh the mechanism of Ross River virus‐induced demyelination is not known, these findings suggest that it is not imnune mediated.