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R C Nowinski

Publications and source records attributed to R C Nowinski.

At least 73 records · Page 4Linked to original sources
PubMed1976

Endogenous oncornaviruses in chemically induced transformation. II. Effect of virus production in vivo.

C3H/HeJ and AKR/J mice differed in their susceptibility to 3-methylcholantrhene (MCA)-induced sarcomagenesis (86% incidence of sarcomas in C3H by 18 wk; 5% incidence in AKR by 18 wk) and in the production of endogenous murine leukemia virus (MuLV) (AKR produced greater than 10(5) plaque-forming units/ml tail extract in XC test; C3H did not produce detectable virus.) A genetic corss between C3H and AKR mice was examined to determine the relationship of virus production to oncogenesis by MCA. Mice of the (C3H X AKR)F X C3H backcross were typed for the production of infectious MuLV by tail biospy and then inoculated with MCA. Of the backcross mice, 81% produced high titers of ecotropic MuLV; the remaining 19% did not contain detectable infectious MuLV. The virus-producing and non-virus-producing backcross mice were equally sensitive and highly susceptible to MCA-induced sarcomagenesis. Tumors of all virus-positive mice contained infectious MuLV. Some tumors (54%) of virus-negative mice also contained infectious MuLV; this indicated the induction of endogenous MuLV in the tumors of these mice. We concluded that the overt production of MuLV in mice of this backcross did not function in the sensitivity of the mice to sarcoma induction by MCA. Furthermore, the presence of virus in some chemically induced tumors was due to an induction pehnomenon independent of the primary oncogenic event.

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PubMed1976

Genetic control of natural immunity to ecotropic mouse leukemia viruses: production of endogenous immunogen.

Mice of the AKR and C57L strains naturally produced low titers of antibody against ecotropic murine leukemia viruses (MuLV). The F1 hybrid of these strains produced anti-MuLV antibody in higher titer than mice of either of the parental strains. Progeny of the genetic backcross C57L X (AKR X C57L)F1 segregated for the production of infectious ecotropic MuLV (according to the Akv-1 and Akv-2 loci) and for the production of antibody against MuLV. All mice that contained infectious MuLV produced anti-MuLV antibodies. Thus, the persistent production of high-titered MuLV in these mice did not result in immunological tolerance towards viral antigens. In contrast, mice that did not contain infectious MuLV could be separated into antibody-producing and -nonproducing classes. The absence of detectable antibody to MuLV in an individual mouse was invariably associated with a virus-free phenotype. Antibody against MuLV reacted primarily with p15 and gp70 proteins of the viral envelope. It was concluded that overt production of endogenous ecotropic MuLV served as a major immunogenic stimulus for the production of anti-MuLV antibody in these mice.

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PubMed1976

Genetic control of natural immunity to ecotropic mouse leukemia viruses: immune response genes.

Humoral immune response to ectropic leukemia viruses in AKR and C57BL/6 mice was controlled by a gene that mapped in linkage group IX. Mice of the AKR strain had an immune nonresponsive allele of this gene, whereas mice of the C57BL/6 strain had an immune responsive allele. Antibody against murine leukemia virus (MuLV) reacted primarily with p15 protein of the viral envelope. It was concluded that the failure to find antibody production in AKR mice was the result of a genetic immunological defect, rather than the result of immunological tolerance that was induced by the persistent viremia of endogenous MuLV.

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PubMed1976

Endogenous ecotropic mouse type C viruses deficient in replication and production of XC plaques.

Endogenous ecotropic type C viruses were induced by iodedeoxyuridine from nontransformed and chemically or spontaneously transformed clones of the C3H/10T1/2 cell line. Viruses produced by cells of certain transformed clones were N-tropic and formed large XC plaques. In contrast, viruses produced by nontransformed C3H/10T1/2 cells were not detectable in the XC plaque test. These XC- viruses infected mouse cells with high efficiency, as shown by the induction of murine leukemia virus group-specific antigens in infected cells, but virus production, as determined by DNA polymerase-containing particles, was extremely low. Upon growth in certain mouse cells these replication-deficient, XC(-) viruses converted to type C viruses that were similar in XC assays to N-tropic AKR virus (XC+).

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PubMed1976

Immune response of the mouse to the major core protein (p30) of ecotropic leukemia viruses.

Sera from normal C57BL/6 mice contained low titers of antibodies against proteins of MuLV. Sera from C57BL/6 mice that were immunized with allogeneic leukemia cells sometimes contained high-titered antibodies against the p15 protein of MuLV; these antibodies detected group-specific antigenic determinants of the p15 protein, since reactions were observed with the p15 proteins of both AKR and Moloney viruses. In contrast, antisera prepared in C57BL/6 mice against the AKR leukemia K36 reacted strongly with the p30 protein of MuLV, as well as with p15. Antibodies in the C57BL/6 anti-AKR K36 sera detected group-specific antigenic determinants of the p30 protein; reactions were observed with the C57BL/6 anti-AKR K36 serum and the p30 proteins of both AKR and Moloney viruses. It was concluded that mice do have the capacity to respond immunologically to antigenic determinants of the MuLV p30 protein, although in most circumstances this is not observed.

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PubMed1975

Lysis of leukemia cells by spleen cells of normal mice.

Spleen cells from 2- to 3-month-old normal mice of some strains having a low incidence of spontaneous leukemia were found to lyse cells of the spontaneous AKR leukemia K36 in the 51Cr release assay. Incubation of 51Cr-labeled ADR K36 cells with spleen cells from normal C57BL/6, C57L, C57BL/10, and RF mice resulted in the release of significantly more 51Cr than that released in the presence of medium alone. In contrast, 51Cr released from AKR K36 cells after incubation with spleen cells from mice of the high leukemic strains AKR and C58 was less than that released spontaneously. The results of competitive inhibition tests when C57BL/6 spleen cells were incubated simultaneously with 51Cr-labeled AKR K36 target cells and varying numbers of nonlabeled cells demonstrated that the cytotoxic activity of normal C57BL/6 spleen cells was directed against an antigen(s) associated with several leukemias, but that was undetectable on normal thymocytes. Pretreatment of C57BL/6 spleen cells with carbonyl iron and a magnet, which removed phagocytic macrophages, did not decrease the cytotoxic acitivity for AKR K36 cells.

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PubMed1975

Anomalous reactions of mouse alloantisera with cultured tumor cells. II. Cytotoxicity is caused by antibodies to leukemia viruses.

Certain alloantisera prepared in mice against H-2 region membrane antigens were found to be unexpectedly cytotoxic for murine sarcoma and leukemia cells in culture. This anomalous cytotoxicity was shown to be the result of antibody in these alloantisera directed against the p15 and gp70 envelope proteins of Mu LV which were present on the surface of the tumor target cells. Sera from aged unimmunized mice of strains used for the preparation of alloantisera also contained antibodies against MuLV protein p15 and gp70 that were cytotoxic for sarcoma and leukemia cells, which indicates that these antibodies occurred naturally in mice. These results independently confirm earlier findings of the widespread occurrence in mouse serum of antibodies reactive with MuLV. The presence of antibody against MuLV in mouse serum which can cause cytotoxic reactions with tumor cells points to the fact that particular caution should be used during the typing of murine sarcomas or leukemias for cell surface antigens, since mouse antisera may yield cytotoxicity (or other serologic reactions) based on anti-MuLV specificities, rather than on anticipated antigens.

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PubMed1973

Cell surface antigens associated with murine leukemia virus: definition of the GL and GT antigenic systems.

Two new serological specificities were identified on the surface of murine leukemia virus (MuLV)-infected cells by direct and absorption immunofluorescence tests. Both antigens were detected with antisera prepared in rats that were growing transplants of syngenic MuLV-induced leukemias. Antigen G(L) was defined with the AKR leukemia K36 as the test cell; antigen G(T) was defined with the W/Fu leukemia C58(NT)D as the test cell. G(L) and G(T) antigens were serologically and genetically independent of the MuLV-induced Gross and G(IX) cell-surface antigens. G(L) and G(T) antigens were found in normal lymphoid cells of mice from high-leukemic strains, but not in lymphoid tissues of mice from most low-leukemic strains. Tumors and leukemias of mice of low-leukemic strains often were G(L) and G(T) positive. Similarly, infection of normal cells with MuLV resulted in expression of G(L) and G(T). With ferritin-labeled antibody the G(L) and G(T) antigens were observed on virus-free segments of the cell surface. Genetically, G(L) and G(T) antigens were each controlled by two dominant unlinked genes in AKR mice; these same antigens were each controlled by three or more dominant unlinked genes in C58 mice. Penetrance of G(L) and G(T) regulatory genes was dependent upon the Fv-1 genotype of the host. Expression of G(L) antigen was closely associated with virus production, whereas expression of G(T) antigen was less closely associated.

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PubMed1972

Serological analysis of the deoxyribonucleic acid polymerase of avian oncornaviruses. I. Preparation and characterization of monospecific antiserum with purified deoxyribonucleic acid polymerase.

Monospecific antiserum was prepared against purified deoxyribonucleic acid (DNA) polymerase from avian myeloblastosis virus (AMV). Immunodiffusion assay with purified DNA polymerase revealed that the anti-DNA polymerase serum formed one precipitation band, whereas no reaction with any of the seven major structural proteins of AMV was observed. The antiserum also demonstrated enzyme-neutralizing antibody activity that was associated with the immunoglobulin G fraction. There was no difference in the neutralization of DNA polymerase activity directed by ribonucleic acid (RNA), DNA, or RNA-DNA hybrid templates.

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