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)

A serologic study was made of five Canadian mouse colonies to determine the prevalence of antibodies to 11 murine viruses. A total of 139 sera from the five colonies were evaluated by complement fixation or hemagglutination inhibition methods. Viral antibodies were present in all five colonies. Antibodies to pneumonia virus of mice, minute virus of mice, Theiler's encephalomyelitis virus, and reovirus type 3 were found in all five colonies. K-virus antibodies were present in four colonies. Polyoma virus antibodies were found in two colonies and Sendai virus antibodies in two other colonies. Mouse hepatitis virus antibodies were present at a low prevalence in three of the five colonies. No antibodies to adenovirus, lymphocytic choriomeningitis virus, and ectromelia were detected in any of the colonies.
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PMID:Serologic study on the prevalence of murine viruses in five Canadian mouse colonies. 20 96

Mouse hepatitis virus (MHV) strain JHM (MHV-JHM) is a neurotropic coronavirus that causes acute fatal encephalomyelitis in 75-99% of infected mice. The surviving animals may subsequently develop demyelinating disease. We compared the S peplomer protein of the wild type (wt) and five temperature-sensitive (ts) mutants of MHV-JHM. In contrast with the wt, none of these five cause fatal disease (mortality less than 10%). Three of these ts mutants did not induce any demyelinating disease, a fourth caused demyelinating disease in 5% of the animals and a fifth, designated ts8, exhibited strong demyelinating properties and caused demyelination in 99% of the animals. SDS-PAGE analysis revealed no differences in the molecular weight of S peplomer protein of wt or ts MHV-JHM mutants. However, isoelectric focusing of the S protein of these five ts mutants and the wt MHV-JHM, followed by transfer to nitrocellulose sheets and immunoblotting with anti-S specific antibody revealed significant differences in the microheterogeneity of the S protein.
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PMID:Microheterogeneity of S-glycoprotein of mouse hepatitis virus temperature-sensitive mutants. 132 26

From 1984 to 1988 one thousand serologic investigations of laboratory animal colonies originating from 10 different European countries were performed. The most prevalent infections in mouse stocks were caused by Mouse hepatitis virus (MHV), Minute virus of mice (MVM), Theiler's encephalomyelitis virus (TEMV), Reovirus type 3 (Reo3), Sendaivirus, and Pneumonia virus of mice (PVM). In mice no infections with Lymphocytic choriomeningitis virus (LCM), Polyomavirus, Mouse adenovirus, and K-virus were recorded. Only two colonies were infected by Ectromelia virus. The first six virus infections of mice were also found in rat colonies as well as the rat-specific Coronaviruses (Sialodacryoadenitisvirus--SDA, Rat corona virus--RCV) and Parvovirus (Kilham rat virus--KRV, Toolan H-1 virus) being endemic. Antibodies to Bacillus piliformis were detectable in about 50% of rat stocks screened. This is in contrast to the mouse, where only about 10% of the colonies were found to be positive. A similar picture was seen for M. pulmonis which is primarily an infection of the rat. In mice no case was detected during the last two years. The number of investigations performed from guineapig, hamster and rabbit colonies was relatively low. Nevertheless, antibodies against the following antigens were detectable: In guineapig stocks: Reo3, PVM, Sendai, Simian virus 5 (SV5) and B. piliformis; in rabbits: Reo3, Sendavirus, SV5, and B. piliformis; in hamsters: PVM, LCM and B. piliformis. The overall contamination rate showed a continuous decrease until 1988. Nevertheless, about 50% of mouse and rat stocks still exhibited antibodies to one or more viral infections.
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PMID:Seromonitoring in small laboratory animal colonies. A five year survey: 1984-1988. 232 35

Mouse hepatitis virus, strain JHM (MHV-JHM), causes a late onset, clinically apparent, demyelinating encephalomyelitis in 40% of suckling C57BL/6 mice born to immunized dams. Suckling mice born to unimmunized dams rapidly succumb to an acute encephalomyelitis. MHV-JHM can be isolated from the brains and spinal cords of maternal antibody-protected mice when the late onset disease becomes clinically apparent, showing that the virus must be present in these mice when they are still asymptomatic. To determine which cells of the central nervous system (CNS) were potential reservoirs for the virus during the asymptomatic period, tissue sections were assayed simultaneously by immunoperoxidase and immunofluorescence staining for the presence of viral antigen and for glial fibrillary acidic protein (GFAP), a marker for astrocytes. The results indicate that 20% (range 0-52%) of the MHV-JHM infected cells in asymptomatic mice were astrocytes. In mice symptomatic with late onset hindlimb paralysis, a higher percentage of infected cells were astrocytes. These results indicate that astrocytes are a target cell in both symptomatic and asymptomatic mice persistently infected with MHV-JHM, and suggest that the astrocyte is a potential cellular reservoir for MHV-JHM in asymptomatic mice.
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PMID:The astrocyte is a target cell in mice persistently infected with mouse hepatitis virus, strain JHM. 284 22

Comparative investigations of Sendai virus, pneumonia virus of mice (PVM), mouse encephalomyelitis virus (mouse polio), minute virus of mice (MVM), and reovirus type 3 (Reo 3) infected murine colonies revealed a 30% higher incidence of positive sera when enzyme-linked immunosorbent assay (ELISA) was employed instead of hemagglutination inhibition (HI) tests. Equivalent sensitivity as in the ELISA was obtained when the same sera were investigated by indirect immunofluorescence (IF) tests. The virus purification techniques described resulted in highly suitable antigens for all indirect ELISA established. Since IIF requires no purified antigens, this test is recommended as an alternative to ELISA as well as to HI and complement fixation (CF) tests for laboratories lacking the necessary equipment for high speed centrifugation. A high incidence of false positive HI reactions was found particularly in Reo 3 routine serology. An updated survey of seromonitoring showed that European murine colonies appeared to be infected far less with Reo 3 if ELISA or IIF tests were employed. During 1982-1984, only 13% of the mouse colonies screened possessed Reo 3 positive sera whereas no natural Reo 3 infection was found in rat colonies. Mouse hepatitis virus (MHV) and the coronaviruses of rats exhibited the highest incidence in murine colonies. A total of 60% of mouse and 41% of rat colonies were found to be infected by these viruses. In comparison with earlier serological surveys, the relative incidence of other murine infections was similar. Antibodies against Bacillus piliformis (Tyzzer's disease) were detected by the IIF test in 41% of the rat colonies screened.
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PMID:Diagnosis of murine infections in relation to test methods employed. 301 10

Mouse hepatitis virus type 4 (MHV-4, the JHM strain), a positive-strand RNA virus of the coronavirus family, is well documented as an inducer of acute and chronic demyelination in mice, as well as subacute demyelination in rats, due to a cytolytic infection of oligodendrocytes. However, experiments to explore the role of virus and host factors in the production of chronic or recurrent demyelinating disease have been limited because MHV-4 usually produces demyelination in conditions that frequently induce a fatal necrotizing encephalomyelitis. To circumvent this problem, we had made and selected mutant viruses that caused both a high incidence of demyelination and a low incidence of encephalitis-induced mortality. One such mutant, designated ts8, consistently caused acute demyelinating disease in over 90% of intracerebrally or intranasally (natural route of infection) inoculated, 4-5 week-old mice from several susceptible strains within 6-10 days. In addition, ts8 typically did not cause fatal necrotizing encephalitis, showing a low mortality (less than 5%). This reflected a unique tropism of ts8 for oligodendrocytes, but a limited one for neuronal cells. We now report that ts8 is also useful for inducing persistent infection of the mouse central nervous system (CNS). The histopathological correlate of this infection is chronic recurrent demyelination, and virus can be demonstrated ultrastructurally in intact oligodendrocytes, in the vicinity of demyelinated areas.
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PMID:Virus persistence and recurring demyelination produced by a temperature-sensitive mutant of MHV-4. 628 82

Mouse hepatitis virus strain JHM (MHV-JHM) causes a chronic encephalomyelitis in susceptible mice, with histological evidence of demyelination in the spinal cord. After intranasal inoculation, virus spreads retrogradely to several brain structures along neuroanatomic projections to the main olfactory bulb. In the absence of experimental intervention, mice become moribund before the spinal cord is infected. In this study, infusions of anti-MHV neutralizing monoclonal antibodies were administered to protect mice from the MHV-JHM-induced acute encephalitis and to allow survival until virus spread to the spinal cord. Under these conditions, virus was observed to enter specific layers (primarily laminae V to VII) in the gray matter of the upper spinal cord, consistent with transneuronal spread. While the brain structures which are the sources for virus spread to the spinal cord cannot be determined with certainty, the ventral reticular nucleus is likely to be important since it is consistently and extensively labeled in all mice and receives projections from subsequently infected areas of the spinal cord. After initial entry into the gray matter, virus rapidly spread to the white matter of the spinal cord. During the early stages of this process, extensive infection of astrocytes was noted, suggesting that cell-to-cell spread via these glial cells is an important part of this process. Reports from other laboratories using cultured cells strongly suggested that astrocytes serve as important regulators of oligodendrocyte function and, by extrapolation, have a major role in vivo in the processes of both demyelination and remyelination. Thus, our results not only outline the probable pathway used by MHV-JHM to infect the white matter of the spinal cord but also, with the assumption that infection of astrocytes leads to subsequent dysfunction, raise the possibility that infection of these cells contributes to the demyelinating process.
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PMID:Spread of a neurotropic coronavirus to spinal cord white matter via neurons and astrocytes. 781 26

Multiple Sclerosis (MS) is an immune-mediated demyelinating disease of humans. Although causes of MS are enigmatic, underlying elements contributing to disease development include both genetic and environmental factors. Recent epidemiological evidence has pointed to viral infection as a trigger to initiating white matter damage in humans. Mouse hepatitis virus (MHV) is a positive strand RNA virus that, following intracranial infection of susceptible mice, induces an acute encephalomyelitis that later resolves into a chronic fulminating demyelinating disease. Immune cell infiltration into the central nervous system is critical both to quell viral replication and instigate demyelination. Recent efforts by our laboratory and others have focused upon strategies capable of enhancing remyelination in response to viral-induced demyelination, both by dampening chronic inflammation and by surgical engraftment of remyelination - competent neural precursor cells.
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PMID:The Biology of Persistent Infection: Inflammation and Demyelination following Murine Coronavirus Infection of the Central Nervous System. 1994 72

Mouse hepatitis virus (MHV) is a positive-strand RNA virus that causes an acute encephalomyelitis that later resolves into a chronic fulminating demyelinating disease. Cytokine production, chemokine secretion, and immune cell infiltration into the central nervous system are critical to control viral replication during acute infection. Despite potent antiviral T-lymphocyte activity, sterile immunity is not achieved, and MHV chronically persists within oligodendrocytes. Continued infiltration and activation of the immune system, a result of the lingering viral antigen and RNA within oligodendrocytes, lead directly to the development of an immune-mediated demyelination that bears remarkable similarities, both clinically and histologically, to the human demyelinating disease multiple sclerosis. MHV offers a unique model system for studying host defense during acute viral infection and immune-mediated demyelination during chronic infection.
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PMID:The pathogenesis of murine coronavirus infection of the central nervous system. 2037 Jun 25

Coronavirus infection of the murine central nervous system (CNS) provides a model for studies of viral encephalitis and demyelinating disease. Mouse hepatitis virus (MHV) neurotropism varies by strain: MHV-A59 causes mild encephalomyelitis and demyelination, while the highly neurovirulent strain JHM.SD (MHV-4) causes fatal encephalitis with extensive neuronal spread of virus. In addition, while neurons are the predominant CNS cell type infected in vivo, the canonical receptor for MHV, the carcinoembryonic antigen family member CEACAM1a, has been demonstrated only on endothelial cells and microglia. In order to investigate whether CEACAM1a is also expressed in other cell types, ceacam1a mRNA expression was quantified in murine tissues and primary cells. As expected, among CNS cell types, microglia expressed the highest levels of ceacam1a, but lower levels were also detected in oligodendrocytes, astrocytes, and neurons. Given the low levels of neuronal expression of ceacam1a, primary neurons from wild-type and ceacam1a knockout mice were inoculated with MHV to determine the extent to which CEACAM1a-independent infection might contribute to CNS infection. While both A59 and JHM.SD infected small numbers of ceacam1a knockout neurons, only JHM.SD spread efficiently to adjacent cells in the absence of CEACAM1a. Quantification of mRNA for the ceacam1a-related genes ceacam2 and psg16 (bCEA), which encode proposed alternative MHV receptors, revealed low ceacam2 expression in microglia and oligodendrocytes and psg16 expression exclusively in neurons; however, only CEACAM2 mediated infection in human 293T cells. Therefore, neither CEACAM2 nor PSG16 is likely to be an MHV receptor on neurons, and the mechanism for CEACAM1a-independent neuronal spread of JHM.SD remains unknown.
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PMID:Murine coronavirus receptors are differentially expressed in the central nervous system and play virus strain-dependent roles in neuronal spread. 2073 37


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