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

Establishment of animal model of virus-induced encephalomyelitis was attempted in strain 13 guinea pigs sensitized with the homologous spinal cord antigen. Intracerebral inoculation of canine distemper virus alone or sensitization with the neural antigen alone did not induce significant clinical signs. Mild histological lesions were found in both the meninges and parenchyma of the central nervous system (CNS) of virus-infected animals, and in the meninges of the sensitized ones. In contrast, combination of virus infection and sensitization resulted in development of neurological signs of CNS disease as well as of marked histological lesions involving both the meninges and parenchyma. The potentiated CNS disease was successfully transferred by the lymph node cells of the sensitized animals into virus-infected ones. These results suggested that the virus-induced lesions in the CNS were potentiated by the lymphocytes sensitized with neural antigen. Depending on the time schedule of the sensitization and virus infection, different courses of CNS diseases including acute, subacute, and/or recurrent ones were induced, indicating the usefulness of this animal model for immunological and virological analysis of virus-induced CNS diseases.
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PMID:Potentiation of neurovirulence of canine distemper virus in guinea pigs by sensitization with neural antigen. 617 11

Theiler's virus infection in mice produces a chronic demyelinating disease which appears to be based on an immune pathogenesis rather than on direct viral destruction of myelin-supporting cells. The purpose of the present study is to ascertain whether viral antigen is present in the cytoplasm of such cells in areas of demyelination. Because of the difficulty of identifying oligodendrocytes in tissues rich in infiltrating mononuclear cells and fixed for immunohistochemistry, I turned to a recently described form of Theiler's virus encephalomyelitis which follows inoculation with the attenuated ww strain and is characterized by extensive spinal cord remyelination by invading Schwann cells and by recurrent demyelination of Schwann cell-remyelinated axons. The unlabeled antibody peroxidase-antiperoxidase technique was employed to study whether such spinal cord Schwann cells were primarily infected by virus at the time when recurrent demyelination was occurring. Whereas other types of cells, including neurons, astrocytes, and macrophages, contained abundant viral antigen, no positive immune reaction was observed in Schwann cells. These results correlate with our previous studies which had suggested that demyelination in this viral model is not dependent on primary viral attack on myelinating cells but is probably dependent on the host immune response.
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PMID:Uncoupled relationship between demyelination and primary infection of myelinating cells in Theiler's virus encephalomyelitis. 627 14

The proteins specified by four Theiler's murine encephalomyelitis virus isolates in infected BHK-21 cells were studied. Their processing, sensitivity to trypsin, and the changeover after viral infection from synthesis of cellular proteins to synthesis of viral proteins were determined by one- and two-dimensional gel electrophoreses. The molecular weights and isoelectric points of the structural and nonstructural proteins of DA and WW isolates, which represent the less virulent subgroup of Theiler's murine encephalomyelitis virus, and of GDVII and FA isolates, which represent the virulent subgroup, were found to be the same. The sensitivity of DA and GDVII isolates to trypsin, as purified virions, and in infected cell extracts was similar. The shut-off of cellular protein synthesis in cells infected with the same two isolates and the changeover to the synthesis of viral proteins appeared to have the same pattern. These findings are interesting since the two subgroups of Theiler's murine encephalomyelitis virus differ in their pathogenicity, intracellular development in infected BHK-21 cells, and RNA composition, as determined by RNase T1 fingerprinting analysis.
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PMID:Proteins induced in tissue culture by four isolates of Theiler's murine encephalomyelitis virus. 630 Apr 15

Viruses have been found to induce inflammatory demyelinating lesions in central nervous system (CNS) tissue of both animal and man, either by natural infections or after vaccination. At least two different pathogenic mechanisms have been proposed for these changes, a cytopathic viral infection of oligodendroglia cells with subsequent cell death, and a host immune reaction against virus and brain antigens. We now report the occurrence of cell-mediated immune reactions against basic myelin proteins in the course of coronavirus infections in Lewis rats. Infection of rats with the murine coronavirus JHM leads to demyelinating encephalomyelitis developing several weeks to months postinfection. Lymphocytes from these diseased Lewis rats can be restimulated with basic myelin protein (BMP) and adoptive transfer of these cells leads to lesions resembling those of experimental allergic encephalomyelitis (EAE) in recipients, which can be accompanied by a mild clinical disease. This model demonstrates that a virus infection in CNS tissue is capable of initiating an autoimmune response which may be of pathogenic importance.
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PMID:Adoptive transfer of EAE-like lesions from rats with coronavirus-induced demyelinating encephalomyelitis. 631 Apr 11

Infection of rats with the murine coronavirus JHM led to acute or subacute encephalitis. Viral and host factors greatly influenced the outcome of the infection. A number of temperature-sensitive (ts) mutants was obtained which differed widely in their capacity to induce lesions of the central nervous system (CNS) in rats. Under defined conditions a subacute demyelinating encephalomyelitis ( SDE ) with pronounced clinical signs was observed 14-160 days post infection (p.i.). A number of rats, which showed a remission of SDE later developed a relapse of the disease accompanied by neurological symptoms. Neuropathological examination of such animals revealed lesions of active demyelination and extended remyelinated areas. The presence of viral antigen or infectious virus in the CNS of these rats demonstrated that they were persistently infected. Further investigations indicated that this virus infection triggers a cell mediated immune response against basic myelin protein which may contribute to the development of subacute to chronic encephalomyelitides .
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PMID:Virological and immunological aspects of coronavirus induced subacute demyelinating encephalomyelitis in rats. 633 Nov 17

Two cases of a very rare complication of rubella i.e. a strictly spinal cord lesion developing during the course of the viral infection, are reported. In the first case, there was a flaccid paraplegia which incompletely regressed after two months. In the second case there were only sensory disorders and sphincter disturbances and recovery was complete after one month. The post-eruption encephalomyelitis lesions are of uncertain paphogenesis but the most common hypothesis suggested is that of a delayed hypersensitivity mechanism involving a cell-mediated immunologic reaction. The prognosis of these post-injection neurologic manifestations is difficult to assess, but spinal cord lesions could have a good prognosis.
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PMID:[2 cases of post-measles myelitis]. 672 35

Demyelination processes due to viral infections (encephalomyelitis induced by mouse hepatitis virus, Theiler's encephalomyelitis, canine distemper, and marek's disease) were simulated in laboratory animals to study the corresponding human diseases (multiple sclerosis, multifocal leucoencephalopathy, Guillain-Barre's syndrome). The following mechanisms of tissue injury are discussed: (1) viral damage of myelin-supporting cells, (2) demyelination occurring as a side effect of specific and non-specific inflammatory reactions to the viruses persisting in the nervous system, (3) autoimmune reaction triggered by virus infection. Special attention is paid to the role of virus agents in the development of these processes.
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PMID:[Demyelinating processes of a viral nature]. 703 82

To the best of our knowledge, the presence of Rieder cells, as a possible expression of a cytopathogenic effect of virus infection in vivo, has not been reported previously. Rieder cells are radially segmented mononuclear cells and were demonstrated in the cerebrospinal fluid (CSF) from a patient with a documented Coxsackie B virus meningo-encephalomyelitis. The Rieder cells were classified enzymatically as promonocytes. DNA-analysis of CSF showed some mitotic activity which, however, might be due to stimulated lymphocytes.
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PMID:Rieder cells in the cerebrospinal fluid from a patient with viral meningo-encephalomyelitis. A case report. 731 47

In 10 of 16 domestic cats with spontaneous non-suppurative encephalomyelitis, lesions were multifocal but relatively few and were considered nonspecific as to cause, although viral agents could not be excluded. Six cats had polioencephalomyelitis or polioencephalitis suggestive of viral infection. The clinical and morphological features are compared with those of previous reports of feline encephalitis possibly of viral origin. Some previously reported epidemiological and serological surveys suggest a possible role for arboviruses.
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PMID:Non-suppurative encephalomyelitis in cats suggestive of a viral origin. 746 77

Theiler's murine encephalomyelitis virus is a neurotropic enterovirus known to cause biphasic neural disease after intracerebral inoculation into adult mice. The present study characterizes a neonatal mouse model with a high disease incidence for the study of the acute phase of the pathogenesis of the DA strain of Theiler's murine encephalomyelitis virus after oral infection. The route of viral spread to and within the central nervous system (CNS) was determined by examining the kinetics of viral replication in various organs and by performing histopathological analysis. Viral antigen was detected widely in the neonatal CNS, mainly in the gray matter, and it was asymmetrical and multifocal in its distribution, with considerable variation in lesion distribution from animal to animal. Necrotizing lesions appeared to expand by direct extension from infected cells to their close neighbors, with a general disregard of neuroanatomical boundaries. The diencephalon showed particular susceptibility to viral infection. Other areas of the CNS, including the cerebellum and dentate gyrus of the hippocampus, were consistently spared. Neurons with axons extending peripherally to other organs or receiving direct input from the peripheral nervous system were not preferentially affected. The kinetics of viral replication in the liver, spleen, and CNS and the histopathological findings indicate that viral entry to the CNS is via a direct hematogenous route in orally infected neonatal mice and that the disease then progresses within the CNS mainly by direct extension from initial foci.
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PMID:Mode of spread to and within the central nervous system after oral infection of neonatal mice with the DA strain of Theiler's murine encephalomyelitis virus. 747 69


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