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)

Utilizing the direct and indirect fluorescent antibody procedure, the antigenic relationship of the feline infectious peritonitis virus (FIPV) to 7 other human and animal coronaviruses was studied. FIPV was found to be closely related to transmissible gastroenteritis virus (TGEV) of swine. Transmissible gastroenteritis virus and FIPV were in turn antigenically related to human coronavirus 229E (HCV-229E) and canine coronavirus (CCV). An interesting finding in the study was that the 8 coronaviruses selected for this study fell into one of two antigenically distinct groups. Viruses in each group were antigenically related to each other to varying degrees, but were antigenically unrelated to coronaviruses of the second group. The first antigenically related group was comprised of mouse hepatitis virus, type 3 (MHV-3), hemeagglutinating encephalomyelitis virus 67N (HEV-67N) of swine, calf diarrhea coronavirus (CDCV), and human coronavirus 0C43 (HCV-OC43). The second antigenically related group was comprised of FIPV, TGEV, HCV-229E and CCV.
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PMID:Antigenic relationship of the feline infectious peritonitis virus to coronaviruses of other species. 8 Oct 44

Mice infected with JHM strain of mouse hepatitis virus develop a demyelinating encephalomyelitis. Myelin sheaths are stripped off axons by invading macrophages after degeneration of the infected oligodendrocytes. The derivation of the virus from granular cytoplasmic particles that condense around and bud into endoplasmic reticulum is demonstrated. The infected oligodendrocytes undergo hypertrophic changes prior to degeneration. Hypertrophic cells are characterized by abundant microtubules, filaments, mitochondria, aggregates of electron-dense particles, and numerous, unusual plasma membrane connections to myelin lamellae. Vacular and hydropic changes are prominent in degenerating cells. The significance of finding infected oligodendrocytes with altered myelin-plasma membrane connections is discussed with reference to the pathogenesis of recurrent, postinfectious demyelination known to develop subsequent to acute virus infections.
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PMID:Oligodendrocytes and their myelin-plasma membrane connections in JHM mouse hepatitis virus encephalomyelitis. 17 79

The mouse hepatitis virus strain JHM was injected intracerebrally into newborn and weanling rats. Three types of diseases were observed: 1. Acute panencephalitis: Almost all suckling rats became moribund within 6 days. Histologically severe panencephalitis with demyelinating foci was noticed; the foci were similar to those found in mice. Virus was easily detectable in the oligodendroglial cells and neurons both by immunofluorescence and electron microscopy. Infectious virus could be isolated. 2. Subacute demyelinating encephalomyelitis (SDE): Three weeks after infection of weanling rats, about 35% of the animals developed paralysis. Neuropathologically, demyelination with a striking predilection for white matter was observed in the brain stem, optic nerve and spinal cord. Virus was detectable by electron microscopy in degenerating oligodendroglial cells only, which corresponded to the results obtained by the immunofluorescent techniques. Infectious virus could be recovered. 3. Chronic progressive paralysis: Inoculated weanling rats without SDE developed 6 to 8 months later a slowly progressing paralysis of the legs. Hydrocephalus and myelomalacia were present. Viral "footprints" could not be detected.
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PMID:Early and late CNS-effects of corona virus infection in rats. 21 26

A 4-month-old, male, healthy dog developed CNS-symptoms 10 days after the second vaccination with live, attenuated distemper and canine hepatitis virus. The animal was euthanized after 2 weeks of illness. Light and electron microscopic examination of the CNS showed a partly necrotizing encephalomyelitis with numberous intranuclear and intracytoplasmic inclusion bodies, and the presence of probable pseudomyxovirus nucleocapsids and of crystalloid and tubuloreticular aggregates. Although there was conformity of inclusion bodies and probable viral structures as revealed by electron microscopy, the latter showed a much wider distribution. In addition, viral structures of a different type were found in polymorphonuclear leukocytes and vascular endothelial cells. Several morphological criteria led to the supposition that they are Picornaviruses, or possibly Arenaviruses. It is thought that their role in the disease process was at best an indirect one.
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PMID:Encephalitis following vaccination against distemper and infectious hepatitis in the dog. An optical and ultrastructural study. 67 89

Intracerebral infection of mice with the neurotropic JHM strain of mouse hepatitis virus usually results in a fatal encephalomyelitis. However, infection with the neutralization resistant mutant, 2.2/7.2-V-2, results in inflammatory cell infiltration of the central nervous system with no apparent clinical symptoms, while conferring resistance to subsequent challenge with a lethal dose of wild type JHMV. The mononuclear cells infiltrating the brains of JHMV variant 2.2/7.2-V-2 infected mice were isolated and characterized. Virus-specific T cells which proliferated in response to JHMV antigen and produced both IL-2 and IFN-g were present among mononuclear cells infiltrating the brain as early as day 5 post-infection. The results suggest that the local immune response within the CNS may be important in dictating the outcome of disease following infections with neurotropic viruses.
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PMID:Virus-specific T cells in the central nervous system following infection with an avirulent neurotropic mouse hepatitis virus. 133 91

The results of a serological survey of a free-living population of meadow voles (Microtus pennsylvanicus) in Pinawa, Manitoba (Canada) showed that these animals possessed antibodies to six of the eleven viruses tested for, namely: reovirus type 3, murine encephalomyelitis agent, ectromelia virus, murine adenovirus, murine hepatitis virus and lymphocytic choriomeningitis virus. The significant increase in the number of individuals possessing specific antibodies suggests that these viruses, or related viruses, may be responsible for the decline in the population studied.
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PMID:[Serological study of the incidence of murine viruses in a population of small wild rodents (Microtus pennsylvanicus Ord, 1815)]. 133 64

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

Theiler's murine encephalomyelitis virus (TMEV) is a picornavirus which induces a chronic demyelinating disease of the central nervous system (CNS) in certain susceptible mouse strains. Demyelination has been shown to result from immunopathological responses mediated by CD4+, major histocompatibility complex (MHC) class II-restricted T cells. As little or no class II is expressed in the normal mouse CNS, the ability of astrocytes to express these proteins and present antigen to T cells from TMEV-infected mice was investigated here. It is shown that astrocytes are capable of presenting TMEV to virus-specific T cells in vitro, and that this ability is dependent on prior induction of MHC class II by interferon-gamma (IFN-gamma) treatment. Unlike other viruses such as murine hepatitis virus-JHM (a coronavirus) and measles, TMEV is not capable of inducing class II on astrocytes directly. There is a correlation between the ease of class II induction on astrocytes from different mouse strains by IFN-gamma and mouse strain susceptibility to TMEV-induced demyelinating disease. These results suggest that following viral infection and initial T-cell infiltration into the CNS, class II induction on astrocytes is a key step allowing local antigen presentation and amplification of immunopathological responses within the CNS and hence the development of demyelinating disease.
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PMID:Susceptibility to Theiler's virus-induced demyelinating disease correlates with astrocyte class II induction and antigen presentation. 162 91

To investigate the antiviral CD4+ T cell response in coronavirus MHV-JHM-induced encephalomyelitis, spleen and thymic lymphocytes from diseased rats were stimulated in culture with virus Ag, expanded and tested for their specificity to viral proteins and nucleocapsid (N) and spike (S) proteins that had been expressed in bacteria. A strong T cell response specific for N was measurable during acute disease, whereas S-specific T cells were only detectable in rats with a later onset of disease. CD4+ T cell lines with specificity for virus and either N or S protein were established and their influence on the course of a mouse hepatitis virus-JHM infection was investigated. All lines were of the CD4+ phenotype. Both N and S protein-specific CD4+ T cells conferred protection to infected Lewis rats and reduced the amount of infectious virus in the central nervous system. After transfer of CD4+ T cells and challenge with virus, an increase in the antiviral IgM response occurred, but neutralizing antibodies were not detectable during the period of virus clearance. Previous CD8+ cell depletion did not abrogate protection mediated by CD4+ T cell line transfer.
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PMID:Nucleocapsid or spike protein-specific CD4+ T lymphocytes protect against coronavirus-induced encephalomyelitis in the absence of CD8+ T cells. 165 90

Mice infected with the JHM strain mouse hepatitis virus (JHMV) develop a fatal encephalomyelitis with evidence of demyelination. It has previously been shown that the adoptive transfer of 5 x 10(7) nylon wool adherent (NWA) spleen cells from immunized donors to lethally infected recipients clears virus from the central nervous system (CNS) and prevents demyelination. Adoptive transfer of a smaller number (1 x 10(7] of NWA spleen cells from immunized donors also protects from death but does not significantly alter virus replication in the CNS during the acute phase of the infection. Moreover, these mice develop a transient non-fatal encephalomyelitis which occurs approximately 3 weeks post-infection. This delayed encephalomyelitis is associated with a mononuclear cell infiltration into the CNS but little or no evidence of virus replication or increased viral antigen. A virus-specific delayed-type hypersensitivity (DTH) response precedes this delayed onset of disease by 24 to 48 h. Resolution of disease correlates with a selective and permanent suppression of the JHMV-specific DTH reactivity. In addition, no virus-specific DTH is detected following adoptive transfer of viral-specific DTH effectors derived from immunized donors. In contrast, these mice respond to a heterologous antigen, KLH, suggesting that the resolution of the encephalitis is accompanied by a profound suppression in viral-specific DTH response.
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PMID:Relapsing encephalomyelitis following transfer of partial immunity to JHM virus. 197 71


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