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)

Protein synthesis in the murine hepatitis virus JHM-infected cells was temporarily inhibited by hypertonic shock. When the cells were returned to isotonic medium the synthesis of six virus-specific polypeptides, 150K, 65K, 60K, 30K, 23K and 14K was reinitiated simultaneously. Polyadenylated RNA isolated from the cytoplasm or polysomes of infected cells was translated in vitro and the products included polypeptides with molecular weights (mol. wt.) of 120,000, 60,000, 30,000, 23,000 and 14,000. Immunoprecipitation and fingerprinting of [35S]methionine-containing tryptic peptides showed that the 60,000 and 23,000 mol. wt. products were identical to the 60K and 23K polypeptides found in infected cells; the 120,000 mol. wt. product showed identity with the 150K intracellular polypeptide and a virus-specific 120K polypeptide synthesized in tunicamycin-treated cells. Two-dimensional polyacrylamide gel electrophoresis strongly suggested that the 30,000 and 14,000 mol. wt. products are equivalent to virus-specific 30K and 14K intracellular polypeptides. [3H]Uridine-labelled polyadenylated virus RNA was isolated from infected cells and sedimented in sucrose gradients containing formamide. The distribution in the gradient of each of the previously identified virus RNAs was determined by gel electrophoresis and gradient fractions enriched for each RNA were translated in vitro. The 120,000, 60,000, 30,000, 23,000 and 14,000 mol. wt. polypeptides were found to be encoded by mRNAs 3, 7, 2, 6, and 4 or 5 respectively. These results demonstrate that the virus-specific polypeptides in JHM-infected cells are encoded in separate subgenomic mRNAs and are translated independently. The assignment of coding functions and the known sequence relationships of JHM RNAs permitted a gene order to be deduced.
J Gen Virol 1983 Jan
PMID:Coronavirus JHM: coding assignments of subgenomic mRNAs. 613 Jan 22

Four major polypeptides with mol. wt. of 22000, 25000, 52000 and 68000 were isolated from solubilized preparations of hepatitis type B surface antigen (HBsAg). These four populations, referred to as P22, P25, P52 and P68, respectively, were used to immunize guinea-pigs. Guinea-pigs were also inoculated with HBsAg and with purified human serum albumin (HuSA). These antisera were utilized to establish that intact HBsAg particles are associated with HuSA antigenic reactivity. HuSA antigenic determinants were associated with purified preparations of P68. HuSA antigenic activity was not detected with purified preparations of P22, P25 and P52 or with respective specific antisera to each of the above. However, purified P68 contained the antigenic determinants of both host protein and hepatitis B virus-specified protein origin.
J Gen Virol 1980 Jun
PMID:Antigenic relationship of a hepatitis B surface antigen-derived polypeptide and human serum albumin. 615 94

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.
J Gen Virol 1981 Oct
PMID:Host cell nuclear function and murine hepatitis virus replication. 617 15

Antibodies were raised in rabbits against the structural components of human coronavirus strain 229E and mouse hepatitis virus strain 3, prepared from disrupted virus particles. Hyperimmune sera to the subcomponents showed cross-reactions by enzyme-linked immunosorbent assay between ribonucleoprotein antigens of these viruses, indicating the presence of a common antigen(s). None of the other virus structural components showed any cross-reactivity.
J Gen Virol 1982 Feb
PMID:Serological relationships of the subcomponents of human coronavirus strain 229E and mouse hepatitis virus strain 3. 617 84

Genome RNA of mouse hepatitis virus (MHV) strain A59 has been used as a template to synthesize two virus-specific probes: cDNArep, representing the majority of sequences of the genome RNA and cDNA3', representing the 3' end of the genome RNA. Molecular hybridization with these cDNAs was used to characterize both genome RNA and intracellular virus-specific RNAs. Hybridization of genome RNAs of MHV strains A59, JHM, and MHV-3 with A59 cDNArep showed that, although these three strains exhibit different pathogenicities, they contain closely related nucleotide sequences. Hybridization of intracellular RNA from MHV-infected cells with virus-specific cDNA shows that (i) the majority of virus-specific RNA is polyadenylated, (ii) virus-specific intracellular RNA contains six subgenomic species of the same polarity as genome RNA and (iii) all subgenomic RNAs contain the same 3' sequences as the genome RNA and thus form a nested set of RNAs.
J Gen Virol 1983 Jan
PMID:Characterization of murine coronavirus RNA by hybridization with virus-specific cDNA probes. 618 31

The antigenic relationship between human cornonavirus strain 229E (HCV 229E) and mouse hepatitis virus strain 3 (MHV 3) was studied by means of the indirect form of enzyme-linked immunosorbent assay (ELISA). A cross-reaction was found with hyprimmune rabbit sera between HCV 229E and MHV 3 which may be due to the adherence of bovine serum componeants from tissue culture media, which were present on virus particles even after extensive purification. No cross-reaction was observed with immune sera absorbed with bovine serum, or with HCV 229E grown in tissue culture without serum. This indirect ELISA with HCV 229E may prove to be useful for studies with human sera.
J Gen Virol 1980 Jul
PMID:Enzyme-linked immunosorbent assay for coronaviruses HCV 229E and MHV 3. 625 92

The ribonucleoprotein (RNP) of avian infectious bronchitis virus (IBV) was examined by electron microscopy after shadowing with carbon/platinum. Linear RNP strands up to 6.7 microns in length, from three IVB strains, were sensitive to both pancreatic RNase and to proteases. These strands were obtained from spontaneously disrupted complete particles but not from disrupted incomplete particles that lacked RNP. They were also released from Nonidet P40-disrupted particles and could be isolated on sucrose density gradients at a density of 1.27 g/ml. In some cases, helical RNP complexes associated with virus particles were observed that were similar to RNPs of human coronavirus strain 229E and mouse hepatitis virus strain 3.
J Gen Virol 1981 Mar
PMID:Ribonucleoprotein of avian infectious bronchitis virus. 626 41

Mouse L fibroblasts infected with mouse hepatitis virus, MHV3, and radiolabelled with 35S-methionine, contained, in addition to the three major structural polypeptides, p24, p56 and p180, two additional ones, p22 and p50. Of these total five polypeptides, only three, p22, p56 and p180, were labelled in infected cells during a 2 min 35S-methionine pulse and are, therefore, presumed to be immediate translation products. Pulse-chases and chymotryptic peptide mapping experiments showed apparent precursor-product relationships between p56 and p50 and between p22 and p24. Protein synthesis in infected cells was synchronized at the initiation stage by pre-exposure to hypertonic medium. Using a 0.5 min pulse-10 min chase sequence, to limit incorporation of 35S-methionine to stretches of approx. 100 amino acids adjacent to translational initiation sites, it was found that all three polypeptides, p22, and p56 and p180 contained radiolabel. It is thus apparent that translation of the three major structural proteins (or precursors) is initiated independently rather than at a single site as in the cases of other positive-strand RNA viruses such as polio or Semliki Forest virus.
J Gen Virol 1981 Jun
PMID:Cellular synthesis and modification of murine hepatitis virus polypeptides. 627 Feb 50

The interaction between mouse hepatitis virus 3 (MHV3) and cells was studied in order to investigate whether or not early events occurring after infection could be involved in the difference in virus replication seen between mouse strains with different genetic sensitivities to MHV3 infection. Kinetic data showed that MHV3 uptake by both macrophages and L cells was time- and temperature-dependent. In addition, treatment of cells with cytochalasin B or prostaglandin E1, prior to virus infection, resulted in a strong inhibition of sheep red blood cell phagocytosis without any effect on MHV3 uptake. Similar uptake of radiolabelled MHV3 was shown by whole spleen cells, purified T lymphocytes and thymocytes. Furthermore, no difference in 3H-labelled MHV3 uptake was seen between macrophages originating from resistant A/J mice, semi-susceptible (C57Bl/6 x A/J)F1 and susceptible animals. These results indicate, therefore, that genetically related in vivo sensitivity toward MHV3 infection is not related to differential uptake of virus by cells.
J Gen Virol 1981 Nov
PMID:Early interaction between mouse hepatitis virus 3 and cells. 627 22

The xenotropic (X-tropic) mouse type C virus (MuLV) and its pseudotype of murine sarcoma virus (MSV) were inoculated into several fertilized developing Pekin duck eggs. The development of the duck embryos was substantially reduced in those receiving the X-tropic viruses compared to eggs inoculated only with tissue culture medium. Infections virus was isolated from some of the adult animals; in others, evidence for integrated virus sequences in the tissues was noted. No specific pathology was found in the ducks that received X-trophic MuLV alone, but one duck developed multiple fibrosarcomas when inoculated at birth with the X-tropic virus pseudotype of MSV. Two ducks receiving X-tropic MuLv had signs of haematopoietic disorders. In addition, more virus-inoculated animals had evidence of hepatitis and encephalitis than control ducks. Antibody production to X-tropic MuLv was present in several ducks inoculated with virus either in embryo or at birth. Absence of antiviral antibodies was noted in those animals whose tissue contained replicating virus. These studies confirm the observations with X-tropic virus in tissue culture. They demonstrate in vivo that avian species are susceptible to infection by the mouse X-tropic virus and that their fibroblasts can be transformed by the X-tropic MuLV pseudotype of MSV.
J Gen Virol 1982 Jul
PMID:Murine xenotropic type C viruses. IV. Replication and pathogenesis of ducks. 628 52


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