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

A combined comparative virological, morphological, and immunological study of experimental coronavirus encephalomyelitis was carried out in mice in order to elucidate the pathogenetic mechanisms involved in the formation of the foci of lesions in acute and chronic forms of the disease. Intracerebral inoculation of C3H mice with the neurotropic JHM strain of murine hepatitis virus induces a disease with demyelinization foci in the CNS running acute, subacute, or chronic course. This model underlies a concept that demyelinating diseases are caused by viruses producing immunopathologic responses realized via certain histocompatibility loci. The long-term persistence of viral antigen in the CNS and liver may be explained by virus replication in hepatocytes and oligodendrocytes at low levels, and exacerbations of the disease are prevented by the immune system.
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PMID:[Experimental coronavirus encephalomyelitis in mice]. 303 10

This study established the feasibility of rederiving numerous mouse hepatitis virus (MHV) and mouse encephalomyelitis virus (MEV) antibody positive strains of mice using cross fostering techniques and a new caging system, thus permitting introduction of virus antibody free mice into a barrier facility. Serologic status of dams within the nucleus breeding colony was determined, and all mice within the breeding colony were housed in individual Microisolator cages. Specific pathogen free (SPF) foster mothers purchased from a commercial source were determined to have no detectable serum antibody to 11 murine viruses including MEV and MHV. Pups delivered naturally from time pregnant dams were cross fostered onto the SPF foster dams. The procedure of cross fostering was conducted within a positive flow, HEPA-filtered, mass air displacement unit within 24 hours of parturition. The virus status of pups from 49 litters was monitored serologically at weaning and again at 6 weeks of age. All cross fostered litters were serologically negative for antibody to mouse hepatitis virus. Seven of 29 litters were negative for MEV antibody titer using this cross fostering technique. Those litters negative serologically to both MHV and MEV (at 3 and 6 weeks) were transferred to a barrier facility and held in isolation. All rederived mice transferred to the barrier facility remained negative for MHV and MEV when sampled at 12 weeks of age.
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PMID:Rederivation of MHV and MEV antibody positive mice by cross-fostering and use of the microisolator caging system. 303 89

In the history of experimental demyelination, allergic encephalomyelitis (EAE) is the most impressive experimental demyelinating disease based on an immunological mechanism. The evolution of the neuropathological process of chronic EAE is very close to that of chronic Multiple Sclerosis. On the other hand experimental inoculation of different viruses can induce various types of demyelination depending on the main target of the virus and the host response, this latter being conditioned by the age, the mechanism of immunity and the persistence of the virus in the brain. The demyelination can be induced by a viral persistent infection primarily affecting oligodendrocytes (CDV, JHM hepatitis virus) or acting through an immunomediate response against myelin (Visna, Theiler virus, human conventional viruses). The experimental demyelinating models show that also in Multiple Sclerosis a viral etiology could be the starting point of a demyelinating process based on a immunologically mediated mechanism.
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PMID:Experimental patterns related to multiple sclerosis pathology. 331 66

The demography and serology of a population of wild meadow voles (Microtus pennsylvanicus) were monitored from 1982 to 1984 near Pinawa, Manitoba, Canada. Serologic tests were performed on 486 samples to detect the presence of viral antibodies to 11 common murine viruses. Meadow voles showed evidence of infection with Theiler's encephalomyelitis, reovirus-type-3, ectromelia, lymphocytic choriomeningitis, adenovirus, and mouse hepatitis viruses. At times of good survival and breeding performance the population was nearly free of evidence of viral infection. During a period of severe mortality in the winter of 1982-1983, evidence of infection by Theiler's encephalomyelitis virus and reovirus-type-3 was obtained. A high prevalence of antibodies and high titers to these two viruses were characteristic of voles that were captured late in the decline in density in the spring of 1983. This association of mortality with a viral outbreak is consistent with the hypothesis that vole population declines are sometimes related to opportunistic pathogens present in the voles' biotic and social environment.
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PMID:Serologic study on the prevalence of murine viruses in a population of wild meadow voles (Microtus pennsylvanicus). 352 73

The murine hepatitis virus, JHM strain, causes a relapsing subacute demyelinating encephalomyelitis in Lewis rats after intracranial infection. The disease process involves both virus persistence within glial cells and the induction of autoimmunological attack of myelin, however, the relative importance of these features involved in chronic relapsing demyelination remains to be determined. In this report, we analyze the tropism of JHM virus to various neural cell types present within primary Lewis rat central nervous system cultures. Infection of primary cultures with JHM virus revealed that type I astrocytes and brain macrophages are the initial target cells of infection and that the myelin-forming oligodendrocytes are comparatively resistant, becoming infected only rarely through virus mediated cell fusion with previously infected cells. In addition, infection of cultures after removal of oligodendrocytes by various means had no effect on the tropism of JHM virus for the cultures. Cytopathic effects of JHM virus proceed rapidly by cell fusion within the astrocyte-macrophage monolayer, leaving the oligodendrocyte population largely unaffected. Therefore, the highly selective infection of type I astrocytes and macrophages appears to form the basis of JHM virus neurotropism in Lewis rats. These results indicate that JHM virus infection of astrocytes and brain macrophages may be more important in inducing chronic relapsing demyelinating processes than direct infection of the myelin-forming oligodendrocytes. Other possible pathways leading to chronic demyelination in rats involving type I astrocytes and brain macrophages are discussed.
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PMID:Analysis of murine hepatitis virus (JHM strain) tropism toward Lewis rat glial cells in vitro. Type I astrocytes and brain macrophages (microglia) as primary glial cell targets. 352 62

Monoclonal hybridoma antibodies directed against the polypeptides of murine hepatitis virus-4 (JHM strain) were tested for their ability to alter the course of a normally lethal intracerebral virus challenge. Three monoclonal antibodies directed against two distinct epitopes on the E2 glycoprotein of MHV-4 protected mice against lethal virus challenge and converted the infection from fatal encephalomyelitis to demyelination. A single neutralizing antibody directed against a third epitope on E2 as well as seven nonneutralizing antibodies to E2, E1, and N polypeptides did not protect against challenge. In mice which received protective antibody, MHV-4 infection was not blocked, however, virus grew to lower titers in liver and brain, and virus replication in the CNS was more restricted than in unprotected mice. Decreased involvement of neurons in the brains of protected mice was observed, and no evidence of neuronal infection in the spinal cords was found. In contrast, oligodendrocytes were infected in the presence of protective antibody, and evidence of demylination associated with mononuclear cell infiltration was found. These studies demonstrate that antibody to a single epitope on a viral glycoprotein can substantially alter the course and phenotype of disease.
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PMID:Murine hepatitis virus-4 (strain JHM)-induced neurologic disease is modulated in vivo by monoclonal antibody. 619 89

The pathogenesis of murine hepatitis virus, strain JHM, was studied in 6- and 12-week-old C57/BL mice. There was 100% mortality in the 6-week-old mice after intracerebral inoculation. The lesions were characterized by necrotizing encephalomyelitis, without demyelination. Intracerebral inoculation of 12-week-old animals, however, resulted in no morbidity or mortality. The 12-week-old animals showed transient virus replication in the brain, spinal cord, and liver, which was cleared by day 14. Histologic examination showed evidence of ongoing demyelination, concomitant remyelination, and hydrocephalus ex vacuo. Although viral antigen was demonstrated by immunofluorescence in the central nervous system of these animals, no infectious virus was recovered, and immunosuppression regimens did not potentiate the disease.
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PMID:Chronic central nervous system demyelination in mice after JHM virus infection. 625 83

Demyelination may be induced by several different pathogenetic mechanisms. We have been utilizing mouse hepatitis virus (MHV) to study virus-induced demyelination in the central nervous system (CNS). To learn whether the different disease phenotypes in 4-week-old mice, caused by wild type (a model for fatal encephalomyelitis) or mutant ts8 (a model for primary demyelination), is due to an altered cellular tropism, we have developed an immunolabeling technique to evaluate critically the localization of MHV antigens in the unique cells of the CNS. Using mouse derived L-cells and primary neuronal cells in vitro, we determined an appropriate fixative (4% paraformaldehyde and 0.5% glutaraldehyde) that both preserved MHV antigenicity and cell structure. These studies in vitro showed the presence of MHV antigens on the surface of cells. Utilizing immunoperoxidase labeling as developed, we studied the localization of MHV antigens in vivo. MHV antigens associated with wild type (wt) virus were localized in neuronal cells as well as oligodendrocytes, which might account for the encephalomyelitis and primary demyelination, respectively. In contrast, MHV antigens associated with ts8 were localized rarely in neurons but commonly in oligodendrocytes. This might account for the uncommon occurrence of fatal encephalomyelitis, but the frequent presence of primary demyelination. Of interest was the finding of viral antigens during MHV infection in the cytoplasmic processes of oligodendrocytes surrounding intact myelin sheaths. We conclude that the different disease phenotypes caused by wt and mutant ts8 reflect differences in the cellular tropism of the two viruses for cells in the CNS.
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PMID:Selective localization of wild type and mutant mouse hepatitis virus (JHM strain) antigens in CNS tissue by fluorescence, light and electron microscopy. 627 37

The model system of central nervous system (CNS) disease induced by mouse hepatitis virus type 4 (MHV-4) is explored by comparison of wild type (wt) MHV-4 and two temperature-sensitive (ts) mutants, designated ts8 and ts15, in BALB/c and SJL/J mice. In BALB/c mice, 3 plaque-forming units (PFU) of wt MHV-4 given intracerebrally caused fatal encephalomyelitis in all mice by 7 days after infection, with spread of virus outside the CNS, especially to liver. In SJL/J mice, 3 PFU of wt virus was cleared within 2-3 days, with little spread, and up tp 100 PFU failed to cause fatal encephalomyelitis. However, larger amounts of virus, like 1000 PFU, caused fatal encephalomyelitis in SJL/J mice. In contrast, 10(4) PFU of MHV-4 ts8 did not cause death in either BALB/c or SJL/J mice, and persisted in the CNS of both strains while retaining its ts phenotype. There was significatnly less spread of virus outside the CNS. BALB/c mice usually showed demyelination, remyelination, and recurrent demyelination with ts8, while SJL/J mice only rarely had lesions. Intracerebral inoculation with 10(4) PFU of MHV-4 ts15 was associated with a persistent infection in CNS and liver of BALB/c mice; however, only occasional demyelination and hepatic lesions occurred. TS15 did not cause death in either BALB/c or SJL/J mice and did not cause histopathologic injury in SJL/J mice.
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PMID:Selected mutants of mouse hepatitis virus type 4 (JHM strain) induce different CNS diseases. Pathobiology of disease induced by wild type and mutants ts8 and ts15 in BALB/c and SJL/J mice. 629 96

Two plaque-size variants of the neurotropic JHM strain of mouse hepatitis virus have been isolated from the virus stock after eight serial passages in suckling mouse brain. One variant, JHM-DL, produces large plaques, while the other, JHM-DS, produces small plaques in tissue culture. DS replicates more slowly, has a lower virus yield in vitro, and is less virulent for mice than DL. They also differ in their pathogenicity for mice: JHM-DL infection results in acute encephalomyelitis while JHM-DS infection results in demyelination. Oligonucleotide fingerprint analysis of the RNA genomes of these two variants revealed that they had almost identical genetic sequences. Each variant, however, had a unique oligonucleotide spot not found in the other. The unique spot of the large plaque variant, JHM-DL, was localized at approximately 3 to 5 kb from the 3' end, while the JHM-DS unique spot was mapped at 14 to 15 kb from the 3' end of the genome. We have further shown that these oligonucleotide changes are not correlated with the plaque morphology. These two viruses may be useful for studying the molecular basis of virus-induced demyelination.
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PMID:Murine coronaviruses: isolation and characterization of two plaque morphology variants of the JHM neurotropic strain. 629 77


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