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

Infection of mice with the JHM strain of mouse hepatitis virus (MHV) results in an acute encephalomyelitis associated with primary demyelination of the central nervous system. Efforts at understanding the components of the immune response in the development of chronic MHV-induced demyelination have implicated the antibody response and both the CD4+ and CD8+ T cell responses. In this report, we demonstrate that Balb/c (H-2d) mice immunized with the JHM (JHMV) strain of MHV develop a CD8+ cytotoxic T lymphocyte (CTL) response. One population of these virus-specific CTL recognize the nucleocapsid (N) protein. Recombinant vaccinia viruses expressing either the entire N protein or carboxy-terminal deletions were used to determine the number and location of the epitope(s) recognized. The CTLs were found to recognize a peptide contained within the carboxy-terminal 149 amino acids of the N protein. Analysis of infected cell lines expressing transfected major histocompatibility genes demonstrated that the anti-N protein CTLs were restricted exclusively to the Ld molecule. These data provide the first definition of a MHV-specific CTL response directed to a viral protein and suggest that the anti-N protein CTL response is one potential mechanism used by the host to clear JHMV from the central nervous system.
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PMID:Mouse hepatitis virus nucleocapsid protein-specific cytotoxic T lymphocytes are Ld restricted and specific for the carboxy terminus. 137 38

Midguts of two strains of the mosquito vector Culex tarsalis were examined by light and electron microscopy following infection with western equine encephalomyelitis virus. Infection of the highly susceptible Knight's Landing strain with high-titered blood meals resulted in pathologic changes in the midgut epithelium after 2-4 days of incubation; lesions included sloughing of epithelial cells into the lumen and necrosis of cells in situ. Infection of Knight's Landing strain mosquitoes with low-titered blood meals and infection of the less susceptible Fort Collins strain with high-titered blood meals did not result in a significant increase in detached luminal cells, with respect to uninfected controls. Sloughing of infected cells into the midgut lumen may contribute to modulation of the mosquito infection. Lesions in the midgut of Cx. tarsalis are inconsistent with traditional views that regarded arbovirus infections of mosquito vectors as non-pathologic. These findings demonstrate that mosquito pathology is not an oddity limited to the previously described interaction between Culiseta melanura and eastern equine encephalomyelitis virus, and suggest that alphaviruses in general may adversely affect their mosquito vectors in nature.
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PMID:Pathologic changes in the midgut of Culex tarsalis following infection with Western equine encephalomyelitis virus. 144 10

Infection of female BALB/c mice with encephalomyocarditis virus results in the development of a paralytic syndrome in 7 to 10 days postinoculation. Previous studies had suggested the involvement of an immune component in the development of central nervous system pathology. We have examined the effects of T-cell depletion on the development of polioencephalitis (neuronal necrosis and inflammation of the brain and brain stem) and the relative contribution of the CD4+ and CD8+ subsets following the establishment of viremia. We show that monoclonal antibody depletion of T cells is effective in the reduction of polioencephalitis when given prior to viral inoculation. However, administration of the antibodies 12 h or more after viral inoculation failed to alter the development of polioencephalitis or encephalomyelitis. We conclude that T cells are involved in the development of central nervous system disease during the initial stages of infection but are not responsible for the later progression of disease.
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PMID:Indirect role of T cells in development of polioencephalitis and encephalomyelitis induced by encephalomyocarditis virus. 167 48

A hybrid vaccinia virus expressing a chimeric protein consisting of thymidine kinase and the encephalitogenic determinant, S1, from guinea pig myelin basic protein was constructed. Infection of guinea pigs with the virus resulted in the development of allergic encephalomyelitis.
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PMID:Viral chimeric protein including a determinant of myelin basic protein is capable of inducing allergic encephalomyelitis in guinea pigs. 172 19

After the isolation of Borrelia burgdorferi, the previously unknown causative agent of Lyme disease, two neurological disorders, Bannwarth's syndrome and acrodermatitis chronica atrophicans-associated neuropathy, which have been known in Europe for decades, gained new interest. With the availability of serodiagnostic tests, a chronic debilitating disorder--progressive borrelia encephalomyelitis--was found to be caused by chronic infection with B. burgdorferi. Beside these typical manifestations, a growing number of publications about various neurological phenomena appeared, which were thought to be caused by B. burgdorferi. This assumption was based in many cases on the results of serodiagnostic tests only. Considerations for causal connections were frequently lacking. While prior to the availability of serodiagnostic tests neurological manifestations of Lyme borreliosis frequently remained undiagnosed, we now face a tendency for overdiagnosis. The great variety of neurological manifestations in Lyme borreliosis--most of them can also be attributed to other conditions--and the high rate of seropositivity for B. burgdorferi amongst the population living in endemic areas require strict criteria for the correct diagnosis of new and typical neurological manifestations.
Infection
PMID:Neurological manifestations of Lyme borreliosis. 180 27

Infection of the mosquito Culiseta melanura (Coquillett) by eastern equine encephalomyelitis virus was examined using transmission electron microscopy (TEM) of whole tagmata and fluorescent antibody assay (FA) and infectious assay (IA) of dissected tissues. Following infectious blood meals from chicks circulating different virus titers, mosquitoes were examined after extrinsic incubation intervals of 1-22 d. Virus was first detected by FA and IA in midguts and nonalimentary tissues 24 h after infection. Nascent virus was first visualized by TEM in several tissues, including midgut, fat body, and salivary glands, of high-titer-infected mosquitoes 48 h after they engorged. Moderate- and low-titer blood meals resulted in slightly slower appearance and dissemination of virus. Results were consistent with dissemination of virus from the posterior midgut to salivary glands via the hemolymph. Neural tissues contained little or no virus, whereas fat body appeared to be an important organ for virus replication and dissemination. Dissemination barriers did not accompany mosquito infections.
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PMID:Patterns of eastern equine encephalomyelitis virus infection in Culiseta melanura (Diptera: Culicidae). 197 15

Infection with the Daniel strain of Theiler's murine encephalomyelitis virus results in immunemediated primary demyelination in the spinal cords of susceptible SJL/J mice. Treatment of chronically infected mice (3 to 7 months) with purified immunoglobulins directed against spinal cord homogenate resulted in an increase in the number and average size of lesions that were undergoing remyelination by oligodendrocytes. In vivo autoradiography with [3H]thymidine demonstrated labeling of many lymphocytes in areas of demyelination and remyelination. A direct correlation was found between number of labeled lymphocytes infiltrating the lesion and size of demyelinating lesions. Remyelinated areas contained proliferating cells that resembled immature oligodendrocytes or progenitor glial cells morphologically. The number of labeled presumptive glial cells correlated with the area of remyelination. However, central nervous system remyelination occurred even in the presence of proliferating lymphocytes and astrocytic hypertrophy. In addition, treatment of normal uninfected SJL/J mice with antiserum to spinal cord homogenate resulted in increased numbers of proliferating cells in the spinal cord. These experiments suggest that immunoglobulins to a spinal cord antigen may induce proliferation of cells in the central nervous system to promote remyelination.
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PMID:Immunoglobulins stimulate central nervous system remyelination: electron microscopic and morphometric analysis of proliferating cells. 200 54

Infection of certain strains of mice with Theiler's murine encephalomyelitis virus results in persistence of virus and an immune-mediated primary demyelination in the central nervous system that resembles multiple sclerosis. Because susceptibility/resistance to demyelination in B10 congeneic mice maps strongly to class I MHC genes (D region) we tested whether expression of a human class I MHC gene (HLA-B27) would alter susceptibility to Theiler's murine encephalomyelitis virus-induced demyelination. Transgenic HLA-B27 mice were found to co-express human and endogenous mouse class I MHC genes by flow microfluorimetry analysis of PBL. In the absence of the human transgene, H-2stf, or v mice but not H-2b mice had chronic demyelination and persistence of virus at 45 days after infection. No difference in degree of demyelination, meningeal inflammation, or virus persistence was seen between transgenic HLA-B27 and nontransgenic littermate mice of H-2f or H-2v haplotype. In contrast, H-2s (HLA-B27+) mice showed a dramatic decrease in extent of demyelination and number of virus-Ag+ cells in the spinal cord compared with H-2s (HLA-B27-) littermate mice. In addition, none of the eight H-2s mice homozygous for HLA-B27 gene had spinal cord lesions even though infectious virus was isolated chronically from their central nervous system. Expression of HLA-B27 transgene did not interfere with the resistance to demyelination normally observed in B10 (H-2b) mice. These experiments demonstrate that expression of a human class I MHC gene can modulate a virus-induced demyelinating disease process in the mouse.
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PMID:Expression of human HLA-B27 transgene alters susceptibility to murine Theiler's virus-induced demyelination. 201 20

A patient with atypical manifestations of Epstein-Barr Virus (EBV) encephalomyelitis is presented. The patient had unusual spinal fluid immunoglobulin abnormalities, the syndrome of inappropriate anti-diuretic hormone secretion, autonomic dysfunction and spinal arachnoiditis. The cisternal CSF, with a very high IgG level (34.3 mg/dl; normal less than 6.1) but a normal albumin content, displayed evidence of massive intrathecal immunoglobulin production. This was further confirmed by the presence of oligoclonal bands. These clinical manifestations have not previously been reported in encephalomyelitis associated with EBV infection.
Infection
PMID:Unusual manifestations of Epstein-Barr virus encephalomyelitis. 184 3

Employing a murine model of multiple sclerosis which utilizes intracranial injection of Theiler's virus murine encephalomyelitis (TMEV) into SJL/J mice, we tested the potential role of tumor necrosis factor alpha (TNF-alpha) in ameliorating CNS demyelination. Infection with TMEV caused early grey matter inflammation (7 days post-infection) in the brain and spinal cord followed by chronic demyelination (35 days post-infection) in the spinal cord. Administration of recombinant human or mouse TNF-alpha starting 12 h prior to infection and then three times weekly had minimal effect on development of grey matter inflammation in the spinal cord. In contrast, TNF-alpha dramatically reduced demyelination present in spinal cord on days 14 and 35 after TMEV infection (P less than 0.01) when compared to controls. CNS virus titers of TMEV were not modified by TNF-alpha administration as measured on days 7, 14, and 35 following infection. In vivo administration of TNF-alpha inhibits TMEV-induced demyelination in susceptible SJL/J mice without affecting virus replication in the CNS.
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PMID:Inhibition of Theiler's virus-induced demyelination in vivo by tumor necrosis factor alpha. 227 4


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