Biological and serological characterization of radiation leukemia virus.

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The serological properties of the gag gene products p15 and p12 of N-and B-tropic viruses of C57BL mice have been examined. Although these viruses were serologically identical by competition assays for proteins gp7l and p30, they were readily distinguishable in competition assays for proteins p15 and p12. Two isolates of N-tropic viruses had pi2s serologically indistinguishable from AKR murine leukemia virus p12, while two Btropic isolates had distinctly different p12s. The latter pi2s were serologically indistinguishable from the p12 purified from the Btropic radiation leukemia virus (RadLV)-/VL-3. Moreover, this p12 was indistinguishable from the p12 of the endogenous C57BL/Ka xenotropic virus. Similarly, the piSs of the B-tropic viruses were serologically distinct from the AKR murine leukemia virus type of p15, as was the p15 of one C57BL N-tropic virus, while another N-tropic isolate had a p15 identical to the AKR murine leukemia virus p15. These results are interpreted to suggest that the endogenous N-tropic virus of C57BL mice undergoes recombination with the endogenous, xenotropic virus and that this mechanism is involved in the generation of B-tropic viruses in C57BL mice.

supporting

confidence: 69%

Serological characterization of B-tropic viruses of C57BL mice: possible origin by recombination of endogenous N-tropic and xenotropic viruses.

Benade¹,

Ihle²,

Declève³

1978

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“…A maximal concentration of 1 X 106 BL/RL12-NP cells per 60-mm dish was maintained by removing some of the super- F T IF RT IF RT IF RT IF in NIH/3T3 (Fv-1 nn) cultures. In this case, however, virus replication was detected by the immunofluorescence or reverse transcriptase assay only after cocultivation of the NIH/3T3 target cells with BL/RL12-NP cells and after the Fv-1 nn cultures had been passaged for [6][7][8][9][10][11][12] cell doublings longer than comparable Fv-1 bb or Fv-1 -/-target cells.…”

Section: Methodsmentioning

confidence: 99%

“…Genetic loci such as Fv-1 (4) and SRV (5) influence host susceptibility patterns. In addition, within a given permissive host, epigenetic, differentiation-specific restriction mechanisms govern the ability of murine type C retroviruses to replicate in certain types of cells but not in others (3,6). Type C viruses with distinctively different cytotropisms have been recovered from mice of strain C57BL/Ka, an Fv-1 bb strain that possesses the dominant allele for the SRV locus (5-7).…”

Section: Introductionmentioning

confidence: 99%

“…Type C viruses with distinctively different cytotropisms have been recovered from mice of strain C57BL/Ka, an Fv-1 bb strain that possesses the dominant allele for the SRV locus (5-7). The radiation leukemia virus (RadLV) and its tissue-culture progeny (RadLV/VL3) induce thymic lymphomas after inoculation into C57BL/Ka hosts, whereas three other isolates, designated BL/Ka(B), BL/Ka(N), and BL/Ka(X), are devoid of leukemogenic activity (6,7). RadLV and RadLV/VL3 are B tropic and thymotropic because they replicate preferentially in thymic lymphocytes of adult mice of Fv-1 bb genotype.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Cytotypically specific transfecting activity of DNA from C57BL/Ka mouse cells producing thymotropic in contrast to nonthymotropic retroviruses.

Kopecká¹,

Declève²,

Lieberman³

et al. 1980

Self Cite

A comparative study has been made of the susceptibility of fibroblastic cells to transfection by DNA from C57BL/Ka mouse lines producing either fibrotropic or thymotropic retroviruses. DNA isolated from fibroblasts that release a B-ecotropic, fibrotropic virus, BL/Ka(B), was found to transfect fibroblasts of Fv-1 bb genotype with release of virus similar to BL/Ka(B). Fv-l DD fibroblasts were also susceptible but expression was delayed, and xenotypic mink lung cells were refractory. In contrast, DNA prepared from a murine T-cell lymphoma line producing a B-ecotropic, thymotropic virus failed to transfect mouse fibroblasts though it transfected a nonproducer T-cell lymphoma line. The data suggest that the Fv-1 and differentiation-specific restriction mechanisms operate at different molecular levels. Genetic susceptibility to type C retrovirus infection has been analyzed in mice of many strains (1-3). Genetic loci such as Fv-1 (4) and SRV (5) influence host susceptibility patterns. In addition, within a given permissive host, epigenetic, differentiation-specific restriction mechanisms govern the ability of murine type C retroviruses to replicate in certain types of cells but not in others (3,6). Type C viruses with distinctively different cytotropisms have been recovered from mice of strain C57BL/Ka, an Fv-1 bb strain that possesses the dominant allele for the SRV locus (5-7). The radiation leukemia virus (RadLV) and its tissue-culture progeny (RadLV/VL3) induce thymic lymphomas after inoculation into C57BL/Ka hosts, whereas three other isolates, designated BL/Ka(B), BL/Ka(N), and BL/Ka(X), are devoid of leukemogenic activity (6, 7). RadLV and RadLV/VL3 are B tropic and thymotropic because they replicate preferentially in thymic lymphocytes of adult mice of Fv-1 bb genotype. The other three viruses were designated fibrotropic to describe their ability to productively infect fibroblasts of appropriate genotype: Fv-1 bb for BL/Ka(B), Fv-1 nn for BL/Ka(N), and nonmurine cells for BL/Ka(X).Virus production has been demonstrated in various cell systems after transfection with DNA purified from cells chronically infected by RNA or DNA viruses (8-10). Transfection of murine fibroblasts by viral DNA obtained from cells infected by retroviruses can shed light on the molecular mechanisms underlying genetic and epigenetic restriction. The initial events during transfection are likely to be different from those of the infective process. Blocks in the infection process could very well be bypassed by transfection. Thus, viral DNA derived from B-and N-tropic virus-infected cells can transfect fibroblasts of either Fv-1 bb or Fv-1 nn genotype, suggesting that Fv-1 genetic control acts at some step that is not shared with the transfection mechanism (11, 12).It was of interest to ascertain whether differentiation-specific restriction operates by a mechanism similar to that of Fv-1 gene restriction. MATERIALS AND METHODSCell Lines and Viruses. The BL-5 and BL-1l cell lines of C57BL/Ka (Fv-1 bb) origin and the NIH/3T3 cell li...

“…Gross (2) and Lieberman and Kaplan (3) subsequently reported the transfer of neoplasia by radiation-induced leukemia virus (RadLV) obtained from radiation-induced leukemias. The extent to which the activation of such viruses plays a role in the etiology of the disease has become an important question (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20). We report studies in mice from which comparisons can be made of genetic factors that influence susceptibility and resistance to leukemia induced by FX or by infection with an isolate of RadLV (the Kaplan strain of RadLV).…”

mentioning

confidence: 99%

Induction of leukemia by both fractionated x-irradiation and radiation leukemia virus involves loci in the chromosome 2 segment H-30-A.

Meruelo¹,

Offer²,

Rossomando³

1983

A common link between the induction of leukemia by (i) fractionated doses of x-irradiation and (ii) radiation leukemia virus in mice may be established by the observation that the segment of chromosome 2. between the loci for the minor histocompatibility antigen H-30 and color coat agouti (H-30-A) includes distinct loci involved in susceptibility to leukemogenesis induced by factors i and ii.Kaplan and Brown (1) first showed that fractionated doses of xirradiation (FX) can cause leukemia in mice. Gross (2) and Lieberman and Kaplan (3) subsequently reported the transfer of neoplasia by radiation-induced leukemia virus (RadLV) obtained from radiation-induced leukemias. The extent to which the activation of such viruses plays a role in the etiology of the disease has become an important question (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20). We report studies in mice from which comparisons can be made of genetic factors that influence susceptibility and resistance to leukemia induced by FX or by infection with an isolate of RadLV (the Kaplan strain of RadLV). MATERTIALS AND METHODSMice, virus, virus inoculation, leukemogenic FX, and antiserum used have been described (21,22).In the cell binding radioimmunoassay, antisera binding to cellular antigens. were measured by indirect radioimmunoassay with "2I-labeled protein A. Mice were bled retroocularly into heparinized tubes, yielding about 0.5 ml of blood, which was treated once with Tris/ammonium chloride to lyse the erythrocytes. The remaining lymphocytes (about 8 X 105) were added to four test tubes, two of which received 50 ,ul of a 1:20 dilution of antiserum against the lymphocyte antigen Ly-11.2, and the others received 50 ,ul of serum diluted 1:20 from unimmunized mice (NMS). Incubation was for 30 min. The cells were diluted with 1 ml of phosphate-buffered saline/fetal calf serum, centrifuged, and resuspended in 50 ,u1 of a 1:10 dilution (2.5 ,ug) of '"I-labeled protein A [specific activity, 1,920 Ci/ mmol (Amersham); 1 Ci = 3.7 X 1010 becquerels] to give 1.5 X 105 cpm per tube. After 30 min at room temperature, the cells were washed three times. The pellets were transferred to new tubes and assayed for radioactivity in a Beckman gamma counter 4000. RESULTS Involvement of Distinct Genes. Recombinant inbred (RI) lines of mice may be used to assess linkage of various genetic loci (23,24). Such RI strains are constructed by crossing two strains of mice and inbreeding F2 offspring to homozygosity (24). Loci that are linked tend to stay in the same initial parental combination (24), and this can be used to infer linkage relationships. We used the CXB/By series (23) of seven RI lines to map loci involved in susceptibility to FX-and RadLV-induced leukemia. These studies demonstrated that distinct genes are involved in susceptibility to leukemia induced by FX and RadLV. For example, some of the RI strains, such as CXBG were highly susceptible to the induction ofleukemia by FX but resistant to induction by RadLV, and some such as CXBD showed th...