Characterization of Murine Coronavirus RNA by Hybridization with Virus-specific cDNA Probes

Weiss, Susan R.; Leibowitz, Julian L.

doi:10.1099/0022-1317-64-1-127

Cited by 22 publications

(17 citation statements)

References 31 publications

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“…We observed a uni- form deletion of approximately 1.5 X 1 O5 Da from the E2 glycoprotein and higher molecularweight subgenomic mRNAs of ATllf cord virus when compared with ATllf and ATlIe brain viruses. Because the E2 mRNA was the lowest molecular weight mRNA with a deletion and because of the nested set arrangement of the coronavirus mRNAs (Stern and Kennedy, 1980a,b;Cheley et al, 1981 a;Weiss and Leibowitz, 1983) one can conclude that the deletion occurred in the coding region of the E2 glycoprotein mRNA of the ATIIf cord virus. The genomic size RNA from wild-type JHM and JHM variants appeared to comigrate (Fig.…”

Section: Comparison Of Mrna and Proteins Synthesized By Jhm Variantsmentioning

confidence: 99%

“…x 1 O6 Da mRNA designated mRNA 7; the genomic size mRNA is called mRNA 1 (Spaan et al, 1981;Wege et a/., 1981). The mRNAs form a 3'-coterminal nested set extending for different lengths in a 5' direction (Stern and Kennedy, 1980a,b;Cheley et al, 1981a;Lai and Stohlman, 1981;Leibowitz et al, 1981;Spaan et al, 1983;Weiss and Leibowitz, 1983). The 5' end of each mRNA not present in smaller mRNA species contains the coding sequence utilized during the infection (Leibowitz et al, 1982;.…”

Section: Introductionmentioning

confidence: 99%

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Characterization of coronavirus JHM variants isolated from wistar furth rats with a viral-induced demyelinating disease

et al. 1989

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Murine hepatitis virus (MHV) can cause neurological disease when inoculated intracerebrally (ic) into mice and rats. Specifically the JHM strain of MHV (MHV-JHM) generally causes an acute encephalitis when inoculated ic into 2-day-old Wistar Furth rats. In contrast, JHM generally produces a chronic demyelinating disease with resulting posterior paralysis when inoculated ic into 10-day-old Wistar Furth rats. In addition, while JHM readily produces a productive infection in a mouse fibroblast cell line (L-2), it does not form syncytia or replicate well in a tissue cell line of glial origin (G26-24). We have isolated and characterized three MHV-JHM viral variants from the central nervous system of two Wistar Furth rats with a MHV-JHM-induced demyelinating disease. The pattern of viral-specific mRNA for all three of these variants differed from what was observed for the wild-type parental MHV-JHM that had been passaged only in tissue culture. One of these variants, ATllf cord virus, which induced a chronic demyelinating disease in 2- or 10-day-old intracerebrally inoculated Wistar Furth rats, had a deletion in the coding region of the peplomer glycoprotein mRNA. In addition, this variant formed massive syncytia and replicated well in G26-24 cells. We have not detected this deletion in the other two JHM variants, ATllf brain virus and ATlle brain virus. ATllf brain virus and ATlle brain virus primarily produced an acute encephalitis when reinoculated into 2- or 10-day-old Wistar Furth rats. In addition, these two variants did not form syncytia and had a reduced ability to replicate in G26-24 cells.

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Section: Comparison Of Mrna and Proteins Synthesized By Jhm Variantsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Characterization of coronavirus JHM variants isolated from wistar furth rats with a viral-induced demyelinating disease

et al. 1989

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“…Infected cells contain five or six subgenomic mRNAs, depending upon the virus studied, and an RNA species which is indistinguishable from genome RNA in structure (Leibowitz et al, 1981;Stern and Kennedy, 1980a, b;Lai et al, 1981). Structural studies have established that the subgenomic mRNAs make up a "nested set" with coterminal 3' ends (Leibowitz et a/., 1981;Stern and Kennedy, 1980a, b;Lai et a/., 1981;Cheley et a/., 1981;Weiss and Leibowitz, 1983;Spaan et al, 1982) and contain a leader sequence of approximately 72 bases at their 5' termini (Spaan et a/., 1983;Lai et a/., 1983Lai et a/., , 1984. This is shown schematically in Fig.…”

Section: Introductionmentioning

confidence: 99%

Detection of a murine coronavirus nonstructural protein encoded in a downstream open reading frame

et al. 1988

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Mouse hepatitis virus (MHV) gene 5 contains two open reading frames. We have expressed the second open reading frame of this gene (gene 5 ORF 2) in an Escherichia coli expression system. This system utilized a plasmid which contained the promoter and the first 36 codons of the recA gene fused in frame with the MHV gene 5 ORF 2, which is fused in turn to the beta-galactosidase gene. The protein product of this gene fusion was used to raise antibody to gene 5 ORF 2. The specificity of the antibody was verified by immunoprecipitation of the in vitro transcribed and translated protein product of gene 5 ORF 2. The second reading frame of MHV gene 5 was shown to be expressed during the course of infection by immunocytochemistry and radioimmunoprecipitation using the antibody raised against the E. coli fusion protein and by two-dimensional gel electrophoresis.

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“…The neurotropic MHV-4 strain showed the highest degree of difference among the strains tested, which also included MHV-2, 3 and A59 (Wege et al, 1981;Weiss and Leibowitz, 1983). Hybridization studies with cDNA clones of the viral RNAs revealed extensive nucleic acid homologies between MHV strains (Cheley et al, 1981;Weiss and Leibowitz, 1983). More recently sequence analyses of the N gene indicated an overall 94% homology between the strongly neurotropic MHV-4 and the weakly neurotropic MHV-A59 (Armstrong et al, 1983;Skinner and Siddell, 1983).…”

mentioning

confidence: 99%

“…In similar analyses with other strains, each MHV isolate yielded a unique oligonucleotide pattern. The neurotropic MHV-4 strain showed the highest degree of difference among the strains tested, which also included MHV-2, 3 and A59 (Wege et al, 1981;Weiss and Leibowitz, 1983). Hybridization studies with cDNA clones of the viral RNAs revealed extensive nucleic acid homologies between MHV strains (Cheley et al, 1981;Weiss and Leibowitz, 1983).…”

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confidence: 99%

Antigenic variation among murine coronaviruses: Evidence for polymorphism on the peplomer glycoprotein, E2

Talbot

Buchmeier

1985

Virus Research

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A panel of 28 monoclonal antibodies (MAb) against the structural proteins of murine hepatitis virus-4, strain JHM (MHV-4) was used in three antigen binding assays to determine the extent of antigenic homology among six strains of murine coronaviruses. The antigenic determinants studied were highly conserved on the E1 glycoproteins and nucleocapsid (N) proteins of all strains tested. In contrast, antigenic polymorphism was observed among the E2 glycoproteins. Of three previously described antigenic determinants against which neutralizing antibodies are directed, only one, termed A(E2), was conserved on all strains. Antigenic site B(E2) was found only on the strongly neurotropic MHV-4 and site C(E2) was present on the virulent MHV-4 and MHV-3 (hepatotropic) strains, but absent on the weakly pathogenic MHV-A59, MHV-1 and MHV-S strains. Four non-neutralizing antibodies against at least one topographically distinct antigenic determinant, which we previously designated D(E2), gave binding patterns consistent with two distinct sites. One of these was present on all MHV strains tested and the other was present on all strains except MHV-S. These non-neutralizing antigenic sites were redesignated E(E2) and D(E2) respectively.

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Characterization of Murine Coronavirus RNA by Hybridization with Virus-specific cDNA Probes

Cited by 22 publications

References 31 publications

Characterization of coronavirus JHM variants isolated from wistar furth rats with a viral-induced demyelinating disease

Characterization of coronavirus JHM variants isolated from wistar furth rats with a viral-induced demyelinating disease

Detection of a murine coronavirus nonstructural protein encoded in a downstream open reading frame

Antigenic variation among murine coronaviruses: Evidence for polymorphism on the peplomer glycoprotein, E2

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