myelin-basic-protein and Coronaviridae-Infections

Topics: Animals; Antibody Formation; Astrocytes; Autoimmune Diseases; Coronaviridae Infections; Encephalomyelitis, Autoimmune, Experimental; Epitopes; Immunity, Cellular; Measles; Myelin Basic Protein; Rats; Rats, Inbred Strains; Time Factors

C57BI/6N mice develop a CNS demyelinating disease when inoculated intracranially at 4 weeks of age with the A59 strain of mouse hepatitis virus (MHV-A59). In order to explore the virus-host interactions, the histological features of the demyelinating disease were correlated with the spatial and temporal distribution of viral transcripts and the expression of oligodendrocyte-specific genes (myelin basic protein, proteolipid protein, myelin-associated glycoprotein, and 2',3' cyclic nucleotide 3'-phosphohydrolase) in the spinal cord of diseased mice. Three distinct phases in the disease were identified. In the first phase, 1 week postinfection (1 WPI), virus replication was widespread in both gray and white matter but was preferentially occurring in glial cells. In the ventral and dorsal root zones where viral transcripts were most abundant, all myelin gene transcripts were decreased before demyelination was seen. During the second phase of the disease (2-3 WPI), viral transcripts decreased in abundance and became restricted to the white matter. Numerous demyelinating lesions were observed and were characterized by inflammatory cells, paucity of oligodendrocytes, and a profound decrease of all myelin gene transcripts. In the third phase of the disease (4-6 WPI) no viral transcripts were detected, and remyelination began. In the lesions and the tissue surrounding them, transcripts of all myelin genes increased to levels above normal. The increased expression of myelin gene transcripts occurred in a synchronized manner and with a cellular distribution reminiscent of that seen in developmental myelination. These molecular events correlated with efficient remyelination and clinical recovery in this murine demyelinating disease.

Topics: Animals; Coronaviridae Infections; Demyelinating Diseases; Gene Expression Regulation; Gene Expression Regulation, Viral; Mice; Mice, Inbred C57BL; Myelin Basic Protein; RNA, Messenger; Spinal Cord

Lewis and Brown Norway rats were infected at different ages with the neurotropic murine coronavirus strain, JHM and the resultant central nervous system diseases were studied. Suckling rats of both strains came down with a fatal, acute encephalomyelitis. Weanling Lewis rats developed a subacute demyelinating encephalomyelitis which neuropathologically revealed changes of an immunopathologic reaction. In contrast, Brown Norway rats developed a clinically silent subacute demyelinating encephalomyelitis with a persistent JHM virus infection which was less severe and quite different from the subacute demyelinating encephalomyelitis in Lewis rats with respect to size, distribution, and localization of the demyelinating plaques as well as the type of infiltrating cells. In addition, infected Lewis rats showed a pronounced lymphocyte proliferation to myelin basic protein and JHM virus whereas lymphocytes from infected Brown Norway rats did not react to these two antigens. These observations demonstrate the pathogenetic importance of host factors in the development of virus-induced demyelination.

Topics: Aging; Animals; Animals, Newborn; Antigens, Viral; Brain; Coronaviridae; Coronaviridae Infections; Demyelinating Diseases; Encephalomyelitis; Immunity, Cellular; Mice; Microscopy, Electron; Myelin Basic Protein; Rats; Rats, Inbred BN; Rats, Inbred Lew; Species Specificity; Spinal Cord

Topics: Animals; Antigens, Viral; Coronaviridae; Coronaviridae Infections; Cross Reactions; Demyelinating Diseases; Encephalomyelitis, Autoimmune, Experimental; Immunity, Cellular; Myelin Basic Protein; Rats; Rats, Inbred Lew; Recurrence