Genetic restriction of murine hepatitis virus type 3 expression in liver and brain: comparative study in BALB/c and C3H mice by immunochemistry and hybridization in situ (original) (raw)
Related papers
Mouse hepatitis virus nasoencephalopathy is dependent upon virus strain and host genotype
Archives of Virology, 1986
Mouse hepatitis virus (MHV) S induced typical MHV spongiibrm 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 genotyoes. 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 offactory tracts, while MHV-A 59, -S and ~IHM 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.
Experimental and Molecular Pathology, 2001
Infection with mouse hepatitis virus (MHV) strain A59 produces and Cavanagh, 1997). Infections with nidoviruses, including acute hepatitis, encephalitis, and chronic demyelination in mice. Howboth coronaviruses and arteriviruses, have been used as ever, little is known about a closely related strain, MHV-2, which is experimental model systems for a variety of neurologic disonly weakly neurotropic. To better understand the molecular basis of neurotropism of MHVs, we compared the pathogenesis and genomic eases . MHV infection of mice is a useful sequence of MHV-2 with that of MHV-A59. Intracerebral injection of laboratory model system for virus-induced demyelination MHV-2 into 4-week-old C57B1/6 mice produces acute meningitis and that mimics many of the pathologic features of multiple hepatitis without encephalitis or chronic inflammatory demyelination. sclerosis Sequence comparison between MHV-2 and MHV-A59 reveals 94-98% sequence identity of the replicase gene, 83-95% sequence identity of Lavi et al., 1984a,b;; Houtman genes 2a, 3, 5b, 6, and 7, and marked difference in the sequence of and Fleming, 1996a,b). Studies of the neurotropic demyelingenes, 2b, 4, and 5a. This information provides the basis for further ating strains MHV-JHM and MHV-A59 provide important studies exploring the mechanism of viral neurotropism and virus-ininsight into the process of CNS infection; however, the mechduced demyelination. ᭧
Virology, 2001
The protein encoded by ORF 4 of mouse hepatitis virus (MHV) is not required for growth of some strains in tissue culture cells, but its role in pathogenesis in the murine host has not been defined previously in a controlled manner. MHV strain JHM causes acute and chronic neurological diseases in susceptible strains of rodents. To genetically manipulate the structural proteins of this and other strains of MHV, we have generalized an interspecies-targeted RNA recombination selection that was originally developed for the A59 strain of MHV. Using this approach, a recombinant MHV-JHM was constructed in which gene 4 was genetically inactivated. Virus lacking gene 4 expression replicated in tissue culture cells with similar kinetics to recombinant virus in which gene 4 expression was not disrupted. Both types of viruses exhibited similar virulence when analyzed in a murine model of encephalitis. These results establish a targeted recombination system for inserting mutations into MHV-JHM. Furthermore, the protein encoded by ORF 4 is not essential for growth in tissue culture cells or in the CNS of the infected host.
Infection and Immunity, 1983
Mouse hepatitis virus type 4 infection of primary glial cultures, which consisted principally of astrocytes (marked by glial fibrillary acidic protein) from encephalitis-susceptible BALB/c or F1 (BALB/c x SJL/J) hybrid mice and resistant SJL/J mice, was studied. Primary neuron cultures from BALB/c and F1 hybrid mice were previously shown to be permissive and were destroyed within 5 days by infection with mouse hepatitis virus type 4, whereas neurons from SJL/J mice were fully resistant. In contrast, in the present study a chronic infection was established and maintained for up to 18 days in glial cultures from all three mouse strains. Infected SJL/J mouse glial cultures produced 10- to 50-fold less infectious virus and showed less cytopathic effect than did cultures from either infected BALB/c or F1 hybrid mice. Cytopathic effect was evident initially in cells from all three strains, and continued virus production occurred in the presence of limited additional cytopathic effect. The...
Experimental Animals, 2003
We previously showed that an intraperitoneal infection with mouse hepatitis virus (MHV) resulted in acute hepatic failure accompanying extremely elevated viral growth in the liver in interferon-γ-deficient BALB/c (BALB-GKO), but not C57BL/6 (B6-GKO) mice. To examine the basis of the strain difference against MHV infection in interferon-γ-deficient mice, viral replication in primary hepatocyte cultures from BALB/c and B6 mice with or without the IFN-γ gene was compared in vitro. The MHV replication in BALB/c hepatocytes with or without the IFN-γ gene was significantly higher than that in B6 hepatocytes with or without the IFN-γ gene, suggesting that there is a strain difference in MHV replication in hepatocytes. Since a significant difference in MHV replication in hepatocytes was not observed between wild type and IFN-γ-deficient mice of the same genetic background, the phenomenon is thought to be independent of IFN-γ. However, pretreatment of hepatocytes with recombinant mouse interferon-γ inhibited MHV replication in a dose-dependent fashion. The results are discussed with respect to the pathology of MHV infection in mice with or without the IFN-γ gene.
Journal of Virology, 1984
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.
Mechanisms of hepatic injury in murine hepatitis virus type 3 infection
1989
In presenting this thesis in partial fulfilment of the requirements for an advanced degree at the University of British Columbia, I agree that the Library shall make it freely available for reference and study. I further agree that permission for extensive copying of this thesis for scholarly purposes may be granted by the head of my department or by his or her representatives. It is understood that copying or publication of this thesis for financial gain shall not be allowed without my written permission.
Mouse susceptibility to mouse hepatitis virus infection is linked to viral receptor genotype
Journal of Virology, 1997
We have reported that the receptor for mouse hepatitis virus (MHV) expressed in MHV-susceptible BALB/c mice (MHVR1) has 10 to 30 times the virus-binding activity of the MHV receptor expressed in MHV-resistant SJL mice (MHVR2) (N. Ohtsuka, Y. K. Yamada, and F. Taguchi, J. Gen. Virol. 77:1683-1992, 1996). This fact indicates the possibility that the difference in MHV susceptibility between BALB/c and SJL mice is determined by the virus-binding activity of the receptor. To test this possibility, we have examined MHV susceptibility in mice with the homozygous MHVR1 gene (R1/R1 genotype), mice with the MHVR1 and MHVR2 genes (R1/R2 genotype), and mice with the homozygous MHVR2 gene (R2/R2 genotype) produced by cross and backcross mating between BALB/c and SJL mice. All 63 F2 and backcrossed mice with the MHVR1 gene (R1/R1 and R1/R2) were susceptible to MHV infection, and all 57 with the homozygous MHVR2 gene (R2/R2) were resistant. We have also examined the MHV receptor genotypes of sever...