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Results for “MOUSE LEUKEMIA VIRUSES”

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At least 19 recordsLinked to original sources
PubMed1980

Different lymphoid cell targets by transformation by replication-competent Moloney and Rauscher mouse leukemia viruses.

Mouse leukemia viruses (MuLV) have been reported to induce tumors involving cells within the T lymphocyte lineage. In the present study, striking differences were demonstrated in the target cells for in vivo transformation by two clonal replication-competent type C viruses, Moloney- and Rauscher-MuLV. Moloney-MuLV-induced tumors and lymphoma cell lines exhibited Thy.1 antigen in the absence of detectable Fc or C3 receptors, indicating their T cell origin. Rauscher-MuLV primary tumors and lymphoma cell lines of the same mouse strain, however, invariably exhibited Fc receptors in the absence of Thy.1 antigen, suggesting that these tumors were of the B lymphoid lineage. The pattern of immunoglobulin synthesis by individual Rauscher-MuLV tumor cell lines was determined by both biosynthetic and radioimmunologic techniques. Rauscher-MuLV lymphoma lines invariably expressed immunoglobulin heavy (mu) chain in the absence of detectable light (kappa or lambda) chains. These findings establish that the target of neoplastic transformation in response to Rauscher-MuLV is an immature cell within the B lymphoid lineage. The demonstration of different target cells for transformation by well characterized clonal strains of mouse leukemia virus should aid in elucidating the mechanisms by which these viruses induce malignancy.

Animals↗
PubMed1975

[In vitro transmission of mouse leukemia virus to restrictive mouse cells: necessity for mixed infection by two different leukemia viruses].

The plaque formation of murine leukemia virus (MuLV) in non permissive mouse cells (N-tropic MuLV in B-type cells, or B-tropic MuLV in N-type cells) was increased by murine sarcoma virus whose plaque-forming activity was extremely low (MuSV XC-). The infection of N-tropic MuLV in B-type cells was increased by MuSV XC- propagated only in N-type cells but not in B-type cells, and the infection of B-tropic MuLV in N-type cells by MuSV XC- propagated only in B-type cells but not in N-type cells.

Cell Line↗
PubMed1969

Mouse leukemia virus: "spontaneous" release by mouse embryo cells after long-term in vitro cultivation.

BALB/c mouse embryo cells maintained in tissue culture on a schedule of rapid transfer at high cell density develop into tumorigenic lines that have lost contact inhibition of cell division. After several months in culture, certain of these lines begin to release mouse leukemia virus. This virus has properties indistinguishable from those of virus found in adult BALB/c mice. The evidence presented here demonstrates that the murine leukemia virus genome must be present in the original embryo cultures. The possibility that the genetic information for making murine leukemia virus is present in a repressed form in every mouse embryo cell is discussed.

Animals↗
PubMed1975

Hybridization of mouse leukemia virus c-DNA to mouse repeated DNA sequences.

Experiments of hybridization between mouse leukemia virus synthetic 3H-DNA probe and mouse main band and satellite DNAs indicate that there is not a higher concentration of viral sequences in the satellite DNA. On the contrary, viral sequences appear to be enriched in the fast renaturing intermediate main band DNA.

Animals↗
PubMed1976

Genetic evidence for a product of the Fv-1 locus that transfers resistance to mouse leukemia viruses.

Extracts of mouse cells have been shown to transfer to N- or B-trophic host range types of mouse leukemia viruses. The genetic specificity of the inhibition was tested in two ways: (i) by correlating the Fv-1 genotype of a number of mouse strains with the restriction-transferring activity of extracts of the respective embryo cell cultures, and (ii) by correlating the Fv-1 genotype of BLC3F2 (C57BL/6 female [Fv-1bb] by C3H male [Fv-1nn] parental strains) mouse embryos, which segregate the Fv-1 alleles in a 12:1 ratio, with the inhibitor activity of extracts of the cells from each embryo. Five independent matings, totaling 45 individual embryos, were tested. Each embryo was cultured, and the Fv-1 genotype was determined independently by titration of N- and B-tropic viruses; the extracts of replicate secondary cultures were tested for their effect on infection of permissive cells by N- and B-tropic viruses. The specific-restriction-transferring activity of the embryos was found to segregate with the appropriate Fv-1 genotype. These res-lts confirm the suggestion that the inhibitor of the leukemia virus host range types in the cellular extracts is a product of the Fv-1 locus.

AKR murine leukemia virus↗
PubMed1978

Relative loss of oncogenic potency of mouse leukemia virus (Gross) after prolonged propagation in tissue culture.

Since the initial development of the "passage A" mouse leukemia virus in 1957, this virus has been propagated in our laboratory by serial passage in newborn C3H(f) mice. At the present time, 10(-2)-10(-3) dilutions in physiological saline solution of this mouse-passaged virus induce lymphatic leukemia in practically all inoculated mice after a latency of 3-5 months. On the other hand, when the same virus was propagated on NIH 3T3 mouse embryo cells in tissue culture for more than 10 years, its leukemogenic potency became considerably reduced. Recent bioassay experiments carried out in our laboratory demonstrated that after such prolonged propagation in tissue culture this virus now induced leukemia in less than 15% of the inoculated suckling C3H(f) mice; only undiluted or 10% dilutions of the tissue culture fluid (very occasionally 10(-2) or 10(-3) dilutions) induced leukemia after a prolonged latency varying from 5.5 to 18 months. The passaged and the tissue-culture-grown virus strains are identical immunologically and indistinguishable in their morphology when examined by electron microscopy. The tissue-culture-grown virus, attenuated in its leukemogenic potency, does not, however, confer immunity against a challenge with the mouse-passaged virus.

AKR murine leukemia virus↗
PubMed1972

Human sarcomas contain RNA related to the RNA of a mouse leukemia virus.

Labeled DNA complementary to the RNA of the Rauscher leukemia virus was hybridized with RNA from the polysome fraction of human sarcomas. Eighteen out of 25 specimens contained RNA possessing homology to the RNA of the mouse leukemia virus but not to that of the unrelated viruses causing mammary tumors in mice or myeloblastosis in chickens. Further, no normal adult or fetal tissues showed significant amounts of RNA specific to mouse leukemia virus. It appears that human sarcomas contain RNA sequences homologous to those found in an agent related to a virus known to cause sarcomas in mice.

Animals↗
PubMed1974

Reciprocal inhibition of mouse leukemia virus infection by Fv-1 allele cell extracts.

Soluble extracts of mouse cells with Fv-1(n) or Fv-1(b) gene alleles specifically and reciprocally inhibit infection of B- or N-tropic mouse leukemia viruses in permissive cell cultures. NB-tropic virus infection was not inhibited by either cell extract. Extracts from Fv-1(-) cells did not inhibit infection by the three virus host-range types, but N- or B-tropic virus infection of Fv-1(-) cells was inhibited by extracts of the nonpermissive cells, and Fv-1(nb) cell extracts inhibited both viruses. The maximum degree of inhibition was 50-80% as determined by immunofluorescent or plaque assays, with extracts containing up to 500 mug/ml of nonpermissive cell protein. The inhibitor(s) is relatively unstable since activity is lost after 2 hr at 37 degrees or 30 min at 56 degrees . The inhibitor(s) was most effective if added 2 hr before or within 2 hr after infection, did not react with the virus directly, inhibit virus attachment, or inhibit the normal cell functions tested. These results indicate that nonpermissive mouse cells contain a product, possibly determined by the Fv-1 gene, which inhibits some early postpenetration event(s) in leukemia virus infection.

Alleles↗
PubMed1978

Genetic control of mouse leukemia virus replication.

The Fv-1 gene of the mouse is a cellular gene, which prevents the replication of murine leukemia viruses. We investigated its intracellular site of action and found that the Fv-1 gene product blocks the appearance of virus-specific RNA in nonpermissive cells, which suggested a transcriptional or a preintegration block. Experiments performed to distinguish between these two possibilities revealed that the Fv-I gene restriction prevents integration of the reverse transcribed proviral DNA into the cell genome. However, we also found that the levels of unintegrated proviral DNA were not significantly affected by the Fv-1 gene restriction soon after infection. These data show that the Fv-1 gene product inhibits a step of the virus life cycle after the synthesis of proviral DNA but before its integration.

Animals↗