Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic infection of susceptible strains of mice with Theiler's murine encephalomyelitis virus (TMEV) results in central nervous system (CNS) demyelination similar to multiple sclerosis. Demyelination induced by TMEV is mediated, in part, by class I-restricted CD8+ T lymphocytes. For these T cells to function, they must recognize virus-infected CNS targets in the presence of class I major histocompatibility complex (MHC) antigen. Therefore, we studied in vivo expression of class I MHC antigen and viral antigen-RNA in prototypic mouse strains that are susceptible (SJL/J) or resistant (C57BL/10SNJ) to TMEV-induced demyelination. In brains of resistant mice, viral antigen-RNA expression peaked on day 3 after infection and was effectively diminished by day 5 such that few virus-infected cells were ever detected in the spinal cord. In contrast, susceptible mice demonstrated delay in clearance of TMEV from the brain and a subsequent increase and persistence of viral antigen-RNA in the spinal cord for as long as 277 days. Viral infection resulted in "upregulation" of class I MHC expression in the CNS. Class I MHC antigens were expressed as early as 1 day after infection in the choroid plexus of both strains of mice before detection of viral antigen or inflammation. In resistant mice, class I MHC expression predominated in the gray matter of the brain and spinal cord on day 7 after infection but returned to undetectable levels by day 28. In susceptible mice, class I MHC expression in the CNS persisted and was intense in the white matter of the spinal cord throughout chronic infection and demyelination. No class I MHC expression was detected in the CNS of uninfected mice. Coexpression of viral RNA and class I MHC antigen was demonstrated in CNS cells by using simultaneous in situ hybridization and immunoperoxidase technique. These results support the hypothesis that a class I-restricted immune response directed against virus-infected cells may be important in the mechanism of demyelination.
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PMID:Coexpression of class I major histocompatibility antigen and viral RNA in central nervous system of mice infected with Theiler's virus: a model for multiple sclerosis. 143 36

We used an in vivo technique to record spinal motor and somatosensory evoked potentials in SJL/J and B10 mice chronically (4-10 months) infected with Daniel's strain of Theiler's murine encephalomyelitis virus (TMEV). SJL/J mice demonstrated primary spinal cord demyelination with chronic TMEV infection, whereas B10 mice were resistant to TMEV induced demyelination. Analysis based on the velocity of the initial peak of evoked responses demonstrated significantly slower conduction velocities in infected SJL/J mice as compared to age-matched uninfected SJL/J controls (p < 0.01) and infected B10 mice (p < 0.01). We noted no significant differences in conduction velocities of spinal evoked potentials recorded between uninfected SJL/J mice, uninfected B10 mice and infected B10 mice. Chronic infection with TMEV in susceptible SJL/J mice is associated with slowed conduction of spinal motor and somatosensory evoked potentials. This sensitive electrophysiologic assay will provide an in vivo method to test therapeutic regimens to inhibit demyelination or promote remyelination.
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PMID:Motor and somatosensory evoked potentials in mice infected with Theiler's murine encephalomyelitis virus. 806 13