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 congenic strain of C3HSS mice, which is histocompatible with C3H mice but differs from them in susceptibility to mouse hepatitis virus (MHV), has been developed by introducing the gene for susceptibility to the MHV-PRI virus from the PRI mice. This was accomplished by continual back-crossing of the hybrids to the C3H mice, but at the same time by selection of susceptibility by use of macrophage culture tests. After 20 back-crosses, a strain homozygous for susceptibility was produced by brother-sister mating of individual mice whose potential for carrying the recessive gene for resistance was tested in progeny. Since the original choice of mice for breeding was based on in vitro macrophage susceptibility, and since highly susceptible mice were developed on the same basis, it seems evident that macrophage susceptibility is an integral aspect of mouse susceptibility. The continued production of almost 50% susceptible mice in the back-crosses is further evidence of the dominant one-locus explanation of genetic susceptibility to this agent. Incomplete penetrance may also be present in 8 and 9 week old mice of the C3HSS strain since there was a sharp decrease in susceptibility of these mice even though their macrophages in culture maintained full susceptibility.
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PMID:Congenic strains of mice susceptible and resistant to mouse hepatitis virus. 13 62

A variant mouse hepatitis virus MHV(C(3)H) to which cultured peritoneal macrophages from both PRI and C(3)H mice were susceptible was isolated from stocks of the MHV(PRI) strain of mouse hepatitis virus. It was cloned on C(3)H macrophage monolayers and killed both adult PRI and C(3)H mice when injected intraperitoneally. This new variant was antigenically indistinguishable from the wild type virus. While the emergence of the variant virus was delayed in the course of infecting C(3)H macrophages with large inocula of MHV(PRI), the second passage grew to a high titer in both cell types without delay. Thus, adaptation to the new host was immediate. Interference, apparently not interferon-mediated, between the two variant viruses may have been the cause for the delay in the emergence of the variant virus. The delayed destruction of C(3)H-cultured macrophages by large inocula of MHV(PRI) uniformly resulted in the emergence of MHV(C(3)H). Whether the new variant emerged as a result of a selection of a pre-existing stable mutant or was conditioned by "growth" in the resistant host was not determined.
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PMID:In vitro interaction of mouse hepatitis virus and macrophages from genetically resistant mice. II. Biological characterization of a variant virus MHV (C3H) isolated from stocks of MHV(PRI). 431 20

Using peritoneal macrophage cultures it was found that both PRI mice and their macrophages in culture were susceptible to mouse hepatitis virus and that C(3)H mice and macrophages were resistant. All F(1) macrophages and some back-cross cell cultures were susceptible. The degeneration of F(1) and back-cross macrophages obtained either from adult mouse peritoneal exudate or newborn mouse liver, occurred more slowly than PRI macrophages. Segregation of susceptibility occurred in the first back-cross generation. Tests of three back-cross generations from susceptible mice yielded about one-quarter of the mice shown to be susceptible either by direct test or test of their macrophages. A clear correlation between susceptibility in vivo and in vitro was established both in the test of the percentage segregation and in tests of individual back-cross mice. A small series of tests, however, indicated that 50 per cent of the back-cross mice had the genetic capacity to transmit susceptibility. Thus a hypothesis of two genes for susceptibility, although not excluded, may yield to a hypothesis of a single dominant gene, incompletely expressed. Resistant cells were converted into susceptible cells by ingestion of a relatively large particle containing a heat-stable substance. This susceptibility, although complete, was temporary. The nature of the factor causing the change has been discussed.
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PMID:The cellular nature of genetic susceptibility to a virus. 1403 Jun 64