Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A group of athymic nude mice developed an unusual chronic wasting disease within 1-3 months after their arrival into the laboratory. Affected nude mice had severe, acute-to-chronic, active hepatitis with multinucleated giant hepatocytes and fibrosis. Vascular and central nervous system lesions were frequently present, giant cell peritonitis, ascites, and multinucleated giant cells in the intestinal epithelial villi were less frequently observed. Mouse hepatitis virus was isolated from the livers of three mice with lesions. The virus, when inoculated into nude mice, produced lesions similar to those observed in the natural outbreak.
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PMID:Naturally occurring mouse hepatitis virus infection in the nude mouse. 19 36

An epizootic of fatal diarrhea occurred in mice which were approximately 10 days of age. The enteric lesions were similar to those reported in lethal intestinal virus of infant mice, but many diseased mice also had necrotic hepatitis. Mouse hepatitis virus antigen was demonstrated in the affected intestine and liver, and a virus that produced syncitium formation in mouse brain tumor cell culture was isolated from the intestines, livers, and brains. The virus was capable of producing intestinal and hepatic lesions similar to the naturally occurring disease after inoculation into suckling mice. Electron microscopy revealed viral particles within affected intestinal epithelial cells of the inoculated mice.
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PMID:Isolation of mouse hepatitis virus from infant mice with fatal diarrhea. 21 Mar 27

An enzyme-linked immunosorbent assay was developed for the detection of antibodies to murine hepatitis virus. A high prevalence of antibody to murine hepatitis virus was found by the enzyme-linked immunosorbent assay in colonies with a low prevalence of complement-fixing antibodies. Murine hepatitis virus strain A59 was found to be broadly reactive as an enzyme-linked immunosorbent assay antigen.
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PMID:Enzyme-linked immunosorbent assay for detection of antibodies to murine hepatitis virus. 23 Oct 52

Murine hepatitis viruses provide excellent animal models for the study of virus-induced diseases of the central nervous system and gastrointestinal tract. Several studies have indirectly provided evidence that the spike glycoprotein (S) of these coronaviruses bears determinants for pathogenesis and the induction of protective immunity. In order to directly evaluate the immunogenicity of this protein, it was purified by affinity chromatography with an in vitro neutralizing and in vivo protective monoclonal antibody which immunoprecipitated the 180-kDa spike glycoprotein of the neurotropic A59 strain of murine hepatitis virus (MHV-A59). Mice immunized twice with approximately 1 micrograms of purified S in Freund's adjuvant developed high titers of neutralizing and fusion inhibiting antibodies, even though the protein was at least partially denaturated after elution from the affinity column. Moreover, these mice were protected from lethal encephalitis when challenged intracerebrally with 10 LD50 of MHV-A59. This study provides a direct demonstration of the importance of the coronavirus spike glycoprotein in the induction of a protective immune response.
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PMID:Protection from lethal coronavirus infection by affinity-purified spike glycoprotein of murine hepatitis virus, strain A59. 215 96

Mouse hepatitis virus and Sendai virus are among the most common viruses naturally infecting laboratory mice. Concanavalin A-stimulated in vitro proliferative responses of splenocytes were examined after infection of BALB/cByJ mice with the JHM strain of mouse hepatitis virus (MHV-JHM) or Sendai virus. Mice were exposed to these viruses by presumed natural routes (per os or intranasally). Immunodepression was marked but transient among BALB/cByJ mice exposed to MHV-JHM. Among mice exposed to Sendai virus and examined over a 21-day period, spleen cells from only one mouse, sacrificed 10 days postinoculation, exhibited a severely impaired ability to respond to concanavalin A. Lymphokine production by spleen cells from control and infected mice was then assessed. IL 2 was either absent or present at very low levels in culture supernates of concanavalin A-unresponsive spleen cells from MHV-JHM-infected mice. Spleen cells from the single Sendai virus-infected mouse also produced very low levels of IL 2. In contrast, IL 1 was detected in supernatants of all spleen cell cultures derived from control, MHV-JHM-infected, or Sendai virus-infected mice. There was not a clear correlation between concanavalin A responsiveness and the ability of spleen cells to produce interferon-gamma. These results stress the importance of using laboratory mice of known microbiological status for immunologic experiments.
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PMID:Altered splenic T cell function of BALB/cByJ mice infected with mouse hepatitis virus or Sendai virus. 243 94

The spread of a neurotropic coronavirus, mouse hepatitis virus strain A59, in the mouse central nervous system was studied after intranasal inoculation. Mouse hepatitis virus strain A59 spread during the 3- to 5-day postinoculation period, through the olfactory pathway into the limbic system. Coronavirus particles were detected in the limbic system by electron microscopy. The combination of temporal propagation through an anatomical-physiological central nervous system pathway and anatomical restriction of viral infection suggests that specific interneuronal transport is important in spread of the virus. This experimental system may represent a model for diseases associated with human coronaviruses (common cold viruses) and/or the human limbic system.
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PMID:Limbic encephalitis after inhalation of a murine coronavirus. 282 81

Mouse hepatitis virus (MHV) S induced typical MHV spongiform lesions in brainstem 28 days following intranasal inoculation of adult A/J, BALB/cByJ, CBA/J, C 3 H/HeJ and C 3 H/RV, but not SJL mice. In all but SJL mice, brain lesions occurred at or near the infectious dose level, based on seroconversion by the indirect immunofluorescence assay. During the acute phase of infection (day 5), lesions were limited to the nose and brain in most genotypes. Exceptions were BALB mice, which had mild hepatitis and SJL mice, which had lesions restricted to the nose. No mortality occurred in any genotype. Following intranasal inoculation of adult mice, MHV-1, -3, -A 59, -JHM and -S all caused brain lesions at 28 days after inoculation. MHV-1 and -3 caused lesions that were usually restricted to the anterior olfactory tracts, while MHV-A 59, -S and -JHM also caused more generalized and pronounced lesions involving the midbrain and pons. These studies suggest that avirulent MHV-S given intranasally to most mouse genotypes is a good model for induction of brain infection in the absence of mortality. They also confirm observations made by others in which MHV-JHM, -S and -A 59 are relatively more neurotropic than other MHV strains, such as MHV-1 and -3.
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PMID:Mouse hepatitis virus nasoencephalopathy is dependent upon virus strain and host genotype. 302 79

Mouse hepatitis virus (MHV)-JHM infection was studied in genetically susceptible (BALB/cByJ) and resistant (SJL/J) mice following intranasal inoculation at 1, 3, 6 or 12 wk of age. Markers of infection included histology, immunohistochemistry, virus quantification and virus serology. All BALB mice developed severe disseminated disease with high mortality due to encephalitis and hepatitis. Peak MHV titers appeared in brain, liver, spleen and intestine on days 3 or 5. Age at inoculation did not influence virus titers in brain, spleen or intestine, but virus titers in liver were inversely proportional to age at inoculation. In 6-wk-old BALB mice, virus was cleared from spleen, intestine and liver by day 30 and from brain by day 60. In intestine, MHV was localized to lymphoid tissue, without fecal excretion. SJL mice of all ages developed remarkably milder disease with low mortality occurring only among mice inoculated at 1 wk of age. SJL mice inoculated at 1 wk had disseminated infection at day 3, but lesions and antigen were cleared from most organs by day 5. Mice inoculated at 3 and 6 wk of age had minimal or no involvement of peripheral organs, and mice inoculated at 12 wk of age had infections restricted to the nose. At day 5, MHV titers in brain, liver, spleen and intestine were significantly lower or undetectable in SJL mice of all ages compared to age-matched BALB mice. In 6-wk-old mice, MHV was cleared from all organs by day 10. Serum antibody titers to MHV were many-fold higher in BALB mice, compared to SJL mice, which mounted only a modest response.
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PMID:Response of genetically susceptible and resistant mice to intranasal inoculation with mouse hepatitis virus JHM. 303 19

Mouse hepatitis virus strain A59 produces chronic central nervous system demyelination in rodents. As late as 6 months after intracerebral inoculation of mice 4 to 6 weeks old, when infectious virus cannot be recovered and viral antigens cannot be detected in the central nervous systems and livers of these animals, primary demyelination is still evident. Using cloned virus-specific DNAs and the highly sensitive and specific technique of in situ hybridization, we have detected low levels of mouse hepatitis virus A59 RNA in the central nervous systems and livers of mice 10 months after inoculation. We suggest that viral persistence may play a role in mouse hepatitis virus A59-induced chronic demyelination.
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PMID:Persistence of mouse hepatitis virus A59 RNA in a slow virus demyelinating infection in mice as detected by in situ hybridization. 608 66

Murine hepatitis virus strains A59 and JHM replicated with equal efficiency in both nucleated and enucleated L2 cells. In addition, treatment of the host cell with either actinomycin D or alpha-amanitin, both inhibitors of host cell RNA synthesis, had no effect on virus replication. Therefore, the replication of murine hepatitis virus did not appear to depend upon either the presence of the host cell nucleus or continued host cell RNA synthesis.
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PMID:Host cell nuclear function and murine hepatitis virus replication. 617 15


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