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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty percent of weanling rats infected with JHM murine corona virus developed a subacute demyelinating encephalomyelitis approximately 3 weeks after intracerebral inoculation. Small demyelinating foci were located in the deep cerebral white matter and large, sharply demarcated demyelinating lesions were detectabll preserved in the demyelinating plaques in areas where the lesions extended to the gray matter. Perivascular cuffings, consisting of plasma cells and mononuclear cells, were frequently found. Viral antigen was found mostly in the white matter and in glial cells, leaving neurons unstained. Electron microscopic studies of the early lesions of white matter disclosed two different kinds of cell degeneration which developed prior to the myelin disruption and mononuclear cell infiltration. One was a small pyknotic cell, which is thought to be an oligodendrocyte and the other is a ballooned cell containing abundant microtubules. Virus particles could be demonstrated only in the latter cell type. Discussion about astrocytes as well as oligodendrocytes was made in relation to the initial stage of demyelination caused by virus infection. This animal model may be useful in the analysis of the mechanisms leading to demyelination in subacute or chronic infections.
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PMID:Corona virus induced subacute demyelinating encephalomyelitis in rats: a morphological analysis. 21 23

The epizootic Trinidad donkey strain of Venezuelan equime encephalomyelitis virus (VEE) was cleared slowly from the circulation of rhesus monkeys following intravenous inoculation, while the live, attenuated vaccine strain, TC-83, was cleared rapidly. The efficent clearance of TC-83 vaccine may be a factor in the lower viremia and benign course of TC-83 virus infection in rhesus monkeys.
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PMID:Vascular clearance of venezuelan equine encephalomyelitis viruses as a correlate to virulence for rhesus monkeys. 41 57

Central nervous system (CNS) lesions were studied from weanling hamsters inoculated with the HBS strain of subacute sclerosing panencephalitis (SSPE) virus. The animals showed clincial signs of acute encephalitis between 8 and 18 days post-inoculation (PI), but all survivors were clinically recovered by day 21 PI. Nevertheless, 13 of 14 hamster brains examined by light and electron microscopy between days 21 and 59 PI had chronic lesions which contained morphologic evidence of persistent viral infection. The lesions developed preferentially in the subependymal areas of the lateral and fourth ventricles and involved degeneration of ependyma with subsequent damage to adjacent parenchyma. All CNS cell types were involved in degeneration. Viral inclusions occurred in both CNS parenchymal cells and in inflammatory cells. Giant cells were particularly common. No budding virus was seen in chronically infected animals, a finding in accord with previous studies. Demyelination was a common constituent of most lesions. It occurred in the presence of inflammatory cells and macrophages, and in later lesions, some remyelination was seen. It is suggested that the damage to myelin is a secondary phenomenon and is not a cellular immune reaction. The possible reasons underlying the latent nature of the virus and the similarities between this condition, canine distemper encephalomyelitis and human SSPE are discussed. It is concluded that the experimental chronic disease is a valid model for the study of human SSPE and may have usefulness in the understanding of other chronic CNS conditions of man, e.g. multiple sclerosis. Additional Key Words: Latent infection; Paramyxovirus; Slow Viruses; Demyelination; Inmmunologic defects; Multiple Sclerosis.
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PMID:Experimental subacute sclerosing panencephalitis in the hamster: ultrastructure of the chronic disease. 61 54

The neurologic complications of varicella-zoster (VZ) virus infections are manifested as zoster with or without CNS involvement, encephalomyelitis, or ocular involvement. Usually the association of VZ virus in these conditions has been determined by finding VZ antibodies in the serum. In a few instances, VZ antibodies have been detected in the CSF. We report two cases of VZ virus infection followed by neurologic complications involving the CNS in which VZ antibodies were present in the CSF. These two cases underscore the need and value of determining the presence of VZ antibodies in the CSF in certain instances.
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PMID:Antibodies to varicella zoster in cerebrospinal fluid. 88 81

Theiler's virus infection in SJL/J mice was studied ultrastructurally at subsequent intervals after intracerebral inoculation. Extensive spinal cord lesions consisting of leptomeningeal and white matter mononuclear cell infiltrates with concomitant primary demylination were seen by 15 days. Stripping of myelin lamellae by invading mononuclear cell processes and vesicular disruption of myelin were demonstrated to be the patterns of myelin breakdown. Oligodendrocytes in the vicinity of demyelinating lesions never showed degenerative changes, and viral inclusions could not be found in any cells in the central nervous system. Remyelinating axons, first detected 21 days after infections, were more frequently seen in the late phase of the disease when conspicuous gliosis was also present. Active demyelination could still be observed as late as one year after infection at which time inflammation was decreased. However, plasma cells were relatively more numerous at later times after infection. These ultrastructural findings are similar to experimental allergic encephalomyelitis, and suggest an immune-mediated mechanism of demyelination in Theiler's virus infection.
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PMID:Primary demyelination in Theiler's virus infection. An ultrastructural study. 120 82

We reviewed the records of 10 children with optic neuritis in whom recovery of vision was poor or incomplete. Our cases were otherwise similar to those described in previous studies in that they were always bilateral, often accompanied by a viral prodrome (seven of 10), and usually associated with disc oedema (seven of 10). Seven of twenty eyes had a final visual acuity of 6/60 or worse and only one patient regained 6/6 vision in either eye. In three patients the best vision in either eye was 6/60 or worse. Recovery of vision was often slow, taking up to six years. Five of 10 patients have developed multiple sclerosis (MS), and one child had acute disseminated encephalomyelitis (ADEM) with optic neuritis. Optic neuritis in children does not always carry a good prognosis for recovery of vision; however, the failure of vision recovery in a short period of time does not necessarily indicate a poor outcome. Some children with optic neuritis develop MS, which can develop even when optic neuritis follows a viral illness.
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PMID:Optic neuritis in children with poor recovery of vision. 129 27

Primary dispersed and organotypic cultures were prepared from selected brain areas and spinal cords of rat (Sprague-Dawley) and mouse (SJL/OLA(F) Ness-Ziona) fetuses and neonates. Following fiber regeneration, synapse formation and myelination, cultures were infected with one of the following viruses: Rabies CVS-21 strain, Sindbis Alphavirus, West-Nile Flavivirus and Theiler Murine Encephalomyelitis virus. Light and electron microscopical studies showed clear differences in the target cells for virus infection; time of viral replication and in the intensity and specificity of the cytopathic effects induced by these viruses. Thus, Sindbis and Theiler viruses induced severe cytotoxicity and demyelination due to rapid viral replication in both neurons and all glial cell types. Rabies and West-Nile viruses, on the other hand, replicated mainly in neurons and at a much slower rate, causing only mild damage to the cells and the myelin sheath. A very specific alignment of West-Nile virions was observed along the interperiod lines of the myelin sheath in several myelinated axons. This peculiar arrangement of the virions, entrapped between the myelin lamellae may lead to a novel concept in the understanding of viral infection.
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PMID:Neuronal cell cultures as a model for assessing neurotoxicity induced by encephalitic viruses. 132 47

Most studies suggest that the pathogenesis of Multiple Sclerosis (MS) is based on immune mechanisms of myelin injury. In addition, a viral infection, possibly established in the first few years of the patient's life, may be crucial in setting the stage for such immune mediated injury when acting on the appropriate genetic background. Of the several models of virus-induced demyelination described in the last two decades, Theiler's murine encephalomyelitis virus (TMEV) infection has emerged as one of the best models for MS.
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PMID:The immunopathogenesis of a viral model of multiple sclerosis: Theiler's virus induced demyelination. 134 36

Theiler's murine encephalomyelitis virus is responsible for a chronic inflammatory demyelinating disease of the central nervous system of the mouse. The disease is associated with persistent viral infection of the spinal cord. Some strains of mice are susceptible to viral infection, and other strains are resistant. The effect of the genetic background of the host on viral persistence has not been thoroughly investigated. We studied the amount of viral RNA in the spinal cords of 17 inbred strains of mice and their F1 crosses with the SJL/J strain and observed a large degree of variability among strains. The pattern of viral persistence among mouse strains could be explained by the interaction of two loci. One locus is localized in the H-2D region of the major histocompatibility complex, whereas the other locus is outside this complex and is not linked to the Tcrb locus on chromosome 6.
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PMID:The interaction of two groups of murine genes determines the persistence of Theiler's virus in the central nervous system. 137 8

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


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