Fusion activity of virions of murine leukemia virus.
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AKR murine leukemia virus↗
Biomedical subjects
D A Zarling
Publications and source records attributed to D A Zarling.
The availability for recognition of normal H-2 antigens by cytotoxic T lymphocytes on a Rauscher-virus-transformed cell, RBL-5A.
The availability for recognition of cell surface H-2Db antigenic determinants on RBL-5A cells in comparison to normal C57BL/L cells was investigated by an in vitro immunological assay. No differences in the immunological recognition of the H-2Db antigens on RBL-5A cells compared to normal C57BL/L cells were detected. This assay system, however, readily detected changes in the H-2Kb determinant profile on target cells from the C57BL/L H-2Kb region mutant strains H(zl) and H(zl70) when compared to normal C57BL/6 mice. The result obtained with RBL-5A target cells therefore suggests that Rauscher murine leukaemia virus transformation does not induce, either genotypically or phenotypically, an immunologically recognizable alteration of the H-2Db antigen profile on this cell.
Animals↗
Association of mouse major histocompatibility and Rauscher murine leukaemia virus envelope glycoprotein antigens on leukaemia cells and their recognition by syngeneic virus-immune-cytotoxic T-lymphocytes.
Physical association was measured between MLV gp70, the envelope glycoprotein of Rauscher murine leukaemia virus (R-MLV), and serologically defined H-2 antigens on the surface of R-MLV transformed C57BL/6 (H-2DbKb) mouse leukaemia cells (RBL-5A). Capping and patching with antisera against H-2Db caused specific co-capping and co-patching of R-MLV gp70 antigens as seen by fluorescence microscopy. Despite the physical proximity of R-MLV gp70 and H-2Db antigens, high titre alphaR-MLV gp70 sera had no effect in blocking syngeneic T-lymphocyte mediated cytolysis of RBL-2A cells whereas alphaH-2Db sera were effective.
Animals↗
Role of sendai virus fusion-glycoprotein in target cell susceptibility to cytotoxic T cells.
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Animals↗
Spontaneous mutations affecting the host range of the B77 strain of avian sarcoma virus involve type-specific changes in the virion envelope antigen.
Previously it was shown that the host-range gene of the Bratislava strain of avain sarcoma virus (B77 virus) spontaneously mutates with a very high rate. The wild-type B77 virus called B77 virus-II, mutates either to virus that efficiently infects duck cells (B77 virus-III) or to virus that does not mutate to the ability to infect duck cells (B77 virus-I) (Zarling and Temin, 1976). No significant differences in either the virion envelope glycoproteins or other major virion proteins were detected by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. However, pseudotypes of B77 virus-I with proteins of a transformation-defective mutant of B77 virus-III formed foci efficiently in duck cells. An alteration in the envelope protein of B77 virus-I was demonstrated by experiments in which B77 firus-I was fused into duck cells with UV-irradiated Sendai virus and formed foci. Neutralization experiments further demonstrated that B77 virus host-range mutants have altered type-specific envelope antigens. Thus, the spontaneous mutations in the host-range gene of B77 virus involve changes in the type-specific virion envelope antigen.
Animals↗
High spontaneous mutation rate of an avian sarcoma virus.
Three genetically distinct types of chicken sarcoma virus Bratislava 77 (B77 virus) differing in their ability to infect duck cells were identified. B77 virus type I does not infect duck cells; B77 virus type II has a low efficiency of infection of duck cells; and B77 virus type III has a high efficiency of infection of duck cells. B77 viruses type I and III are produced by spontaneous mutation during the growth of B77 virus type II in chicken cells. The spontaneous mutation of B77 virus type II TO B77 virus type III occurs with a high rate (approximately 1 mutation per 50 infected cell generations), requires cell replication, and neither occurs during the synthesis of viral DNA on an RNA template nor during the transcription of progeny viral RNA from the provirus. The rate of spontaneous mutation of B77 virus type II to B77 virus type I is greater than the rate of spontaneous mutation of B77 virus type II to B77 virus type III.
Animals↗
Spontaneous mutation of RNA tumour viruses.
There are 2 categories of spontaneously occurring avian and mammalian RNA tumour virus mutants: conditional and non-conditional. 1) Conditional mutants are able to replicate in or transform cells only under certain physiological conditions or in certain cells. RNA tumour virus temperature-sensitive mutants, focus-morphology mutants, and host range mutants are spontaneously formed. Some of these conditional mutants probably arise by point mutations in the viral genome. 2) Non-conditional mutants have genetic lesions that render them inactive under all conditions. There are non-conditional spontaneous RNA tumour virus mutants that are missing either the virion envelope glycoprotein or both the envelope glycoprotein and the virion DNA polymerase. These mutants cannot replicate or transform cells. Other spontaneous non-conditional mutants can replicate but are defective in their ability to transform fibroblastoid cells. These spontaneous transformation-defective mutants can have deletions in 10-20% of the genomic RNA. Conditional mutants with an altered host range occur at a high rate of approximately 1 mutation/50 infected cell generations during DNA-to-DNA information transfer. This type of conditional mutation requires cell replication but does not occur frequently either during the original synthesis of viral DNA (RNA-to-DNA information transfer) or during the transcription of progeny viral RNA from the (RNA-to-DNA information transfer) or during the transcription of progeny viral RNA from the DNA (DNA-to-RNA information transfer). Temperature-sensitive and focus-morphology mutants also have a high rate of spontaneous formation. Non-conditional mutants missing the viral envelope glycoprotein, DNA polymerase, or transformation gene, also appear to be spontaneously formed at a high rate. Normal avian and mammalian cells contain RNA tumour virus-related genes in their DNA. It is hypothesized that these endogenous RNA tumour virus-related genes in normal cells also have a high rate of spontaneous mutation and are involved in neoplastic processes.
Animals↗