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At least 19 recordsLinked to original sources
PubMed1975

Cell-surface antigens induced by Friend and Rauscher virus complexes and their associated lymphatic leukemia viruses in the rat.

The WKA/Mk rat tumors induced by Friend virus complex, Rauscher virus complex, and their associated lymphatic leukemia viruses were investigated for their antigenic relationhips with transplantation experiments and cytotoxicity tests. It was found that Friend lymphatic leukemia virus-induced tumors lacked part of the tumor-associated transplantation antigens (TATA's) on Friend virus complex-induced tumors, and the former did not express the type-specific (Friend) TATA for the latter not shared by Rauscher virus complex-induced tumors, which was previously reported by the authors. In contrast, the antigenic differences between TATA's of Rauscher virus complex-induced tumors and those of Rauscher lymphatic leukemia virus-induced tumors were not clearly demonstrated. Furthermore, these studies indicated that Rauscher lymphatic leukemia virus-induced tumors had a weak type-specific TATA not shared by the tumors induced by Friend lymphatic leukemia virus. These results of transplantation studies were also serologically supported by cytotoxicity tests.

Absorption↗
PubMed1977

Solubilized TSTA and the major viral structural proteins, gp70 and p30, in the immune response to murine leukemias induced by Friend and Rauscher virus.

Antigens present in gp70 and p30 purified from Rauscher virus, were tested for immunogenicity in various assays measuring the anti-tumor immune response against lymphocytic leukemias of Friend (FBL-3) or Rauscher (RBL-5) virus origin. p30 had no effect on in vitro cytotoxicity against tumor cell targets mediated by either an anti RBL-5 serum or lymphocytes from animals immunized with FBL-3 cells. gp70 had had no effect on serum-mediated cytotoxicity but used at high concentrations it inhibited cell-mediated cytotoxicity. When used to immunize mice directly against subsequent challenge with the RBL-5 and FBL-3 leukemias, p30 had no discernible effect, while gp70 afforded partial protection against RBL-5 but only at high concentrations. Cell-free preparations of tumor membranes containing negligible amounts of gp70 were antigenically superior to gp70 in both the in vitro and in vivo assays. It is concluded that antigens on these purified proteins that are also expressed on tumor cells are not major targets of the anti-tumor immune response in this system.

Animals↗
PubMed1977

Growth of bone marrow cells of normal and Rauscher virus infected mice in suspension cultures stimulated by CSA.

Bone marrow cells of normal and Rauscher virus (RLV) infected CBA/J mice were cultured under stimulation by postendotoxin serum. Cellular morphology and the number of granulocytic committed stem cells from day 1-5 after the onset of the cultures were studied with different amounts of postendotoxin serum added. There was a good correlation between total cellularity, the number of immature granulocytopoietic cells and the number of colony forming unit cells (CFUc) in suspension with the amount of postendotoxin serum. Postendotoxin serum delayed the appearance of macrophages in the cultures for 1-2 days. Cells from RLV infected animals showed a rather normal differentiation of the morphological recognisable cells 5 and 21 days after infection, but the CFUc survival in vitro 3 and 5 weeks after infection was reduced.

Animals↗
PubMed1976

In vitro differentiation of Rauscher-virus-induced myeloid leukemia cells.

Three cell lines were established in vitro from myeloid leukemias of C57Bl/6 strain mice which had been inoculated with Rauscher virus at birth. The use of heated conditioned medium from peritoneum proved helpful for the initial growth of leukemic cells. At early in vitro passage levels, cell line R433 differentiated only to macrophages after contact with conditioned medium from peritoneum but it appeared to have lost the ability to differentiate during an extended period of cultivation. Cell line R448 was cytologically promyelocyte. When exposed to conditioned medium, this cell line differentiated only to neutrophilic granulocytes. Cell line R453 maintained the ability to differentiate either to neutrophilic granylocytes or to macrophages. Single cells recloned three times still gave rise to both types of mature cells containing conditioned medium. Occasional cases of "spontaneous" differentiation in clonal lines of R453 also occurred.

Animals↗
PubMed1979

Erythropoietin responses and physical characterization of erythroid progenitor cells in Rauscher virus infected BALB/c mice.

Infection of BALB/c mice with Rauscher leukemia virus (RLV) gives rise to pronounced erythrocytopoiesis manifesting in splenomegaly and is associated with progressive development of anemia. In the spleen erythroid colony forming units (CFU-E) increase exponentially up to 800-fold that of normal levels by the third week of infection. In vitro these CFU-E are dependent on erythropoietin for colony formation, their erythropoietin requirements being higher than that of CFU-E from normal mice. Numbers of CFU-E in spleen and degree of splenomegaly in anemic RLV infected mice were also shown to be modified by red blood cell transfusion, but progression of the disease was not stopped. Erythroid burst forming units (BFU-E) were also responsive to erythropoietin. However, a small proportion of cells also formed BFU-E colonies at concentrations which did not support growth of normal marrow BFU-E. When compared to normal, CFU-E found in RLV-infected spleen have similar velocity sedimentation rates. However, buoyant density separation of leukemic spleen cells indicated that CFU-E were more homogeneous (modal density 1.0695 g/cm3) than CFU-E from normal spleen. Analysis of physical properties of CFU-E and the nonhemoglobinized erythroblast-like cells, which accumulate in the spleen showed that they differed mainly in their distribution of cell diameter. Our findings show that erythroid progenitor cells in RLV infected mice are responsive to erythropoietin in vitro. Also in vivo erythropoiesis appears to be under control of erythropoietin but other factors which lead to progression of RLV disease apparently exist. Most proerythroblast-like cells, which are characteristic of this disease, apparently lack the potential to form colonies and may be more mature than CFU-E.

Animals↗
PubMed1979

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↗
PubMed1976

Reverse transcriptase activity per virion for avian myeloblastosis virus and Rauscher murine leukemia virus.

We have measured reverse transcriptase enzyme activity per virus particle for samples of avian myeloblastosis virus (BAI strain) and murine leukemia virus (RAUSCHER) USing the synthetic template poly(rC)-oligo(dG). Absolute virus concentrations were determined directly by laser beat frequency spectroscopy. Enzyme activity per virion was determined from the slope of the activity plotted as a function of virus concentration. With this reverse transcriptase assay, the minimum activity (expressed as picomoles of dGTP incorporated/virion per hour) is estimated at (28.1 +/- 4.2) X 10(-7) for avian myeloblastosis virus and (1.1 +/- 0.2) X 10(-7) for murine leukemia virus. The sensitivity of this assay, which is determined by the level of incorporated radioactivity measurable above background, is 2.5 X 10(-4) virions for avian myeloblastosis virus (with dGTP specific activity of 8.9 Ci/mmol) and 88 X 10(-4) virions for murine leukemia virus (with dGTP specific activity of 6.52 CI/mmol). These results show that although reverse transcriptase assays can obviously be used to measure relative virus concentrations of equally purified samples of the same virus, they can be very misleading when used to compare the concentrations of different virus species.

Avian Leukosis Virus↗
PubMed1976

Method for reproducible large-volume production and purification of Rauscher murine leukemia virus.

Rauscher murine leukemia virus was produced in roller-bottle cultures of chronically infected JLS-V9 cells. Virus from this culture fluid was concentrated and purified by two semi-isopycnic bandings in sucrose gradients. Virus material obtained from young, nonconfluent cultures (early-harvest virus) yielded products characteristically containing endogenous ribonucleic acid-dependent deoxyribonucleic acid polymerase with high specific activity (400 to 1,000 pmol of [3H]thymidine 5'-triphosphate incorporated per milligram of protein per hour). Fluids obtained from older confluent cultures (late-harvest virus) yielded products with endogenous ribonucleic acid-dependent deoxyribonucleic acid polymerase with little or no specific activity (200 pmol or less of [3H]thymidine 5'-triphosphate incorporated per milligram of protein per hour), but with higher virus particle counts and greater amounts of protein and gs antigen than the early-harvest products.

Cell Line↗
PubMed1976

A fucose-deficient glycoprotein precursor to Rauscher leukemia virus gp69/71.

Rauscher leukemia virus glycoprotein gp69/71 is synthesized in virus-infected cells by way of a 90,000 dalton glycoprotein precursor, termed Pr2a+b. This precursor could be labeled with radioactive glucosamine and methionine but not with fucose; whereas gp69/71 could be detected by labeling with radioactive glucosamine, fucose, or a mixture of amino acids but seemed to be deficient in methionine relative to Pr2a+b. Pr2a+b and gp69/71, were specifically precipitated by an antiserum prepared against phosphocellulose purified Rauscher gp69/71. Other virus-specific precursors, in addition to Pr2a+b, could be precipitated by antiserum prepared against detergent disrupted virus. Neither Pr2a+b nor gp69/71 was precipitated from cell extracts by antisera to Rauscher p30. Tryptic maps of Pr2a+b and gp69/71 showed that these glycoproteins share many tryptic peptides. Pulse-chase experiments with 14C-labeled amino acids indicated that gp69/71 was not radio-labeled during the pulse-labeling period but slowly appeared during the chase incubations. Pr2a+b, however, was rapidly labeled and tended to disappear during long chases. Furthermore, two nonglycosylated viral proteins, termed p15E and p12E, are structurally related to Pr2a+b. Viral p15E and p12E contained the same methionine-containing tryptic peptide fraction as Pr2a+b as determined by ion-exchange chromatography. These results provide evidence that Pr2a+b is a precursor to gp69/71 and establish a structural and possible precursor-product relationship between Pr2a+b, p15E, and p12E.

Amino Acid Sequence↗
PubMed1975

Attempts to transform murine hemopoietic cells by Rauscher leukemia virus.

Primary Rauscher leukemia virus (RLV)-induced myeloid leukemias can produce many small clones in agar in the absence of a factor needed for the proliferation of normal myeloid cells. It seems that leukemic cells can more efficiently utilize the small amount of colony-stimulating factor (CSF) that is produced by them. At optimal stimulation by exogenous CSF, leukemic cells exhibit a poorer rate of proliferation than normal bone marrow cells. Hemopoietic cells can replicate the virus after infection in vitro. In some experiments, infection of normal bone marrow cells leads to the production of some cells with the same growth pattern as cells from primary leukemias.

Animals↗
PubMed1978

Structural studies on Rauscher murine leukemia virus: isolation and characterization of viral envelopes.

A preparative method for isolating pure viral envelopes from a type-C RNA tumor virus, Rauscher murine leukemia virus, is described. Fractionation of virions of Rauscher murine leukemia virus was studied after disruption of the virions with the detergents sodium dodecyl sulfate of Nonidet P-40 in combination with ether. Fractionation was performed through flotation in a discontinuous sucrose gradient and, as appeared from electron microscopic examination, a pure viral envelope fraction was obtained in this way. By use of sensitive competition radioimmunoassays or sodium dodecyl sulfate-polyacrylamide gel electrophoresis after immunoprecipitation with polyvalent and monospecific antisera directed against Rauscher murine leukemia virus proteins, the amount of the gag and env gene-encoded structural polypeptides in the virions and the isolated envelope fraction was compared. The predominant viral structural polypeptides in the purified envelope fraction were the env gene-encoded polypeptides gp70, p15(E), and p12(E), whereas, except for p15, there was only a relatively small amount of the gag gene-encoded structural polypeptides in this fraction.

Ether↗