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At least 19 recordsLinked to original sources
PubMed1978

Viral gene expression in murine sarcoma virus(murine leukemia virus)-infected cells.

NIH 3T3 cells infected with Moloney murine sarcoma virus (murine leukemia virus) produce virions which contain about 99% murine sarcoma virus RNA and 1% murine leukemia virus RNA. This report describes experiments which measured intracellular concentrations of proviral DNA and RNA transcripts for each of the viruses. We found that three to four copies of proviral DNA from each virus were integrated into the cellular DNA. Measurements of RNA specific for each of the genomes by hybridization to specific cDNA reagents revealed a 10- to 15-fold difference in concentration in both nuclear and polysomal RNA fractions, with murine sarcoma virus RNA predominating in both cases. Unless there are major differences in stability between the two viral RNAs, our results suggest that transcriptional control is responsible for much of the difference in final levels of virus synthesis.

Cell Line↗
PubMed1975

Heat sensitivity of murine sarcoma virus.

Murine sarcoma virus (Moloney) was found to be heat labile. Inactivation curve represents a first-order kinetics at temperatures between 30 degrees and 60 degrees. Inactivation constant analysis showed an inflexion at about 45 degrees, and the activation energy was calculated as 67.6 kcal/mol for higher temperature range and 7.95 kcal/mol for lower temperature range. Nature of inactivation is also discussed.

Culture Media↗
PubMed1979

Thermolabile protein kinase molecules in a temperature-sensitive murine sarcoma virus pseudotype.

Murine sarcoma virus-associated protein kinases that bind to actin have been purified by affinity chromatography on actin coupled to Sepharose. Heat inactivation studies showed the presence of thermolabile enzyme activity in pseudotypes containing a temperature-sensitivity mutant of murine sarcoma virus (MSV) but not in two independent wild-type MSV pseudotypes. Studies with Sephadex G-75 column fractions showed that a low molecular weight form, approximately 15,000, is the major thermolabile kinase in the temperature-sensitive MSV virions. Antibodies raised against the MSV-coded p60 protein, when added to the in vitro reaction mixtures, showed specific phosphorylation of the IgG heavy chain and a simultaneous reduction in the extent of phosvitin phosphorylation catalyzed by the various MSV pseudotype kinases. Thus a transforming retrovirus-coded enzyme activity that interacts directly with a major cytoskeletal protein and whose activity parallels the transforming ability of a conditional MSV mutant has now been identified.

Actins↗
PubMed1976

An improved assay for feline leukaemia virus pseudotypes of murine sarcoma virus.

An assay is described for feline leukaemia virus pseudotypes of murine sarcoma virus which increased the virus titre by about 100-fold over conventional assays. The titre is independent of dilution and no secondary focus formation occurs. The assay may be used to study virus neutralization and to detect and type feline leukaemia virus in feline embryo cells by interference.

Adsorption↗
PubMed1977

Pathology of neoplasms and other lesions induced in rats with Moloney murine sarcoma virus.

Moloney murine sarcoma virus (M-MSV) was injected directly into the fetuses of Sprague-Dawley rats during the late stage of gestation and into the neonates within 24 hours after birth. Ninety rats developed 188 neoplastic lesions during the 8-week period of observation. Nearly all of the neoplasms were of mesenchymal derivation. Sixty percent of these neoplasms revealed more complex histologic features than those previously reported for neoplasms induced in rodents with M-MSV and were designated "malignant mesenchymoma" which developed preferentially in the proximal parts of the extremities, distant from the inoculation site. Rhabdomyosarcoma and osteosarcoma which developed in a pure form at the various sites were the next most common tumor type. Osteosarcoma developing in a pure form and as a component of malignant mesenchymoma in the humerus and femur was comparable to that of juxtacortical osteosarcoma of man; The development of excessive bones were observed in the forelimb and/or hind leg, suggesting a type of skeletal malformation. The reaction to M-MSV merits attention as a model for the study of an osteosarcoma and malignant mesenchymoma as well as rhabdomyosarcoma and also for the study of viral teratogenesis in man, as "rubella syndrome".

Animals↗
PubMed1979

Phenotypically distinct target cells for murine sarcoma virus and murine leukemia virus marrow transformation in vitro.

An in vitro hematopoietic microenvironment was established from explained fragments of bone marrow from adult noninbred NIH Swiss mice with the use of corticosteroid-reconstituted horse serum. Infection with Kirsten murine sarcoma virus (Ki-MuSV) with either a Rauscher murine leukemia virus (R-MuLV) or Balb:virus-1 helper virus coat reduced proliferation of granulocytic and pluripotent hematopoietic stem cells and produced neoplastic transformation of both macrophages and preadipocytes in the adherent cell population within a 4-week period. Ki-MuSV-transformed, virus-releasing macrophages formed clusters of 4-49 cells in 0.8% methylcellulose-containing medium in the absence of added colony-stimulating factor (CSF), synthesized lysozyme, ASD-chloroacetate substrate-specific esterase-M, and CSF, and produced tumors following inoculation iv into adult NIH Swiss mice or ip into newborn NIH Swiss mice. In cultures infected with helper leukemia viruses R-MuLV or Balb:virus-1, gradual transformation of a distinct cell phenotype was observed over a 9-week period with generation of increasing numbers of atypical myeloblasts and promyelocytes which showed dyssynchronous nuclear-cytoplasmic maturation, basophilic granulation, cytoplasmic vacuolation, and formation of incompletely maturing CSF-dependent granulocyte-macrophage colonies in vitro and small spleen colonies in vivo. These data demonstrated that rapid biologic expression of the murine sarcoma virus genome in specific adherent "stromal" marrow cells prevents detection of a more subtle helper-virus-induced dysmyelopoiesis in a distinct nonadherent cell population.

Animals↗
PubMed1975

Adaptation of N-tropic Friend leukaemia virus and its murine sarcoma virus pseudotype of non-permissive B-type C57BL/6 mouse cell line.

N-tropic Friend leukaemia virus (FLV) was serially passaged in a B-type C57BL/6 mouse cell line, YH-7. After a single passage, the infectious efficiency of FLV in the restrictive YH-7 cells was significantly increased. This adapted character of FLV could be reversed by a single passage in permissive N-type MLg cells. The true host range conversion from N to NB was accomplished after eleven to twelve passages in YH-7 cells. In contrast, the host range conversion of N-tropic murine sarcoma pseudotype, MuSV(FLV), took place after two passages.

Adaptation, Biological↗
PubMed1978

Further evidence for deletion of envelope glycoprotein (gp69/71) sequences in formation of Moloney-murine sarcoma virus.

Moloney-murine sarcoma virus (S+L- strain of M-MSV) has been nonproductively cloned in murine and non-murine host cells (S+L- cells) and the expression of Moloney leukaemia virus (M-MuLV) 30000 mol. wt. core protein (p30) and envelope glycoprotein (gp69/71) were studied by radioimmunoassay. Antigenic determinants of the M-MuLV p30 were associated with the sarcoma virus genome in these non-productively transformed cell clones studied, while the determinants of M-MuLV gp69/71 were not. The absence of envelope-associated glycoprotein expression in sarcoma virus transformed cells was confirmation of biological studies demonstrating that rescued sarcoma virions acquire envelope-associated properties of host range, neutralization and interference from rescuing helper virus, and further evidence that the M-MuLV gp69/71 sequences have been deleted during the formation of the M-MSV. During the course of these studies, it was also found that S+L- dog cells were releasing into culture supernatant large amounts of the p30 antigenic determinant, apparently as a soluble antigen.

Cell Line↗
PubMed1979

Orthotopic bone induction at sites of Moloney murine sarcoma virus inoculation in mice.

Moloney murine sarcoma virus (M-MSV) induces at the site of inoculation in newborn and adult mice and rats various types of sarcoma, including osteosarcoma. The induced tumours are fatal in newborn, whereas sarcomas developed in adult animals regress spontaneously. The regression is mediated mainly by a cellular response. We have now demonstrated that the presence of sarcomas induced by M-MSV is a powerful stimulus for periosteal osteogenesis around tumour masses. Orthotopically induced osteogenesis by M-MSV may serve as a model for local regulation of bone growth and for cell differentiation studies, and may help explain the aetiology of some human bone disorders.

Animals↗
PubMed1976

The pathology of brain tumors induced by murine sarcoma virus, Moloney strain.

Murine sarcoma virus, Moloney strain, was inoculated intracerebrally into 75 Spraque-Dawley rats within 24 hours after birth. Of 48 rats examined histologically within 35 days after virus inoculation, most developed granulomatous lesions in the meninges or in the cortex and in the glial nodules of the subependymal region, or in all these regions. The granulomatous lesions first appeared 8 days after virus inoculation and reached a peak about 30 days after virus inoculation. Thereafter, the lesions healed gradually to scars and disappeared. Of 27 rats that survived beyond 35 days, 10 developed brain tumors at or near the sites of cortical granulomatous lesions and subependymal glial nodules. The interval from virus inoculation to death of tumor-bearing rats was between 40 to 115 days, averaging 84 days. The predilection sites were in the subependymal region and hippocampal cerebral cortex. Three brain tumors were cultured using monolayer and rotation culture techniques. These cultured tumor cells showed morphological features very similar to those of the original tumor cells. THe tumor was classified morphologically into the astrocytoma group by light and electron microscopy and by cytological characteristics of tumor cells in tissue culture.

Animals↗
PubMed1979

Radiation induction of endogenous type C virus from mouse cells transformed in vitro by murine sarcoma virus.

Cell lines from AKR and BALB/c mouse embryos were compared for their sensitivity to X-ray induction of endogenous type C virus. K-Balb cells, a Balb/3T3 cell line nonproductively transformed by Kirsten murine sarcoma virus, were found to be sensitive to X-irradiation. At a dose as low as 50 R, X-rays induced virus expression in K-Balb cells, and the induction frequency increased with increasing dose of X-rays up to 400 R. Among two classes of inducible endogenous viruses carried by K-Balb cells, only Balb:virus-2 was activated by X-irradiation, whereas both Balb:virus-1 and Balb:virus-2 were activated after the cells were treated with 5-iodo-2'-deoxyuridine. UV light and 4-nitroquinoline 1-oxide were also shown to induce virus expression in K-Balb cells. The virus-induction frequency for these physical and chemical carcinogens was much lower (approximately 3 times 10(-4)) than that for 5-bromo-2'-deoxyuridine (approximately 1 times 10(-1)).

4-Nitroquinoline-1-oxide↗
PubMed1979

Induction of lytic plaques by murine leukemia virus in murine sarcoma virus-transformed nonproducer mouse cells persistently infected with mouse hepatitis virus MHV-S.

Kirsten murine sarcoma virus-transformed, nonproducer BALB3T3 (K-BALB) cells were persistently infected with mouse hepatitis virus, MHV-S. The cultures developed plaques after infection with murine leukemia viruses. If the murine leukemia virus-infected cultures were further submitted to the UV-XC assay, comparable numbers of XC plaques were obtained. The sensitivity to murine leukemia viruses, as determined by the UV-XC assay, was higher in MHV-S-infected cells as compared to uninfected K-BALB cells.

Animals↗
PubMed1978

Studies with the baboon endogenous virus and its pseudotype of murine sarcoma virus in marmosets.

Three marmoset species (Saguinus oedipus oedipus, S. fuscicollis, Callithrix jacchus) failed to show evidence of infection or disease following inoculation of baboon endogenous type-C virus (BaEV). Cells infected with a Kirsten murine sarcoma-BaEV pseudotype (MSV[BaEV]) produced a progressive fibrosarcoma in S. o. oedipus and tumors in S. fuscicollis and C. jacchus which regressed. Tumor formation is believed to be due to growth of inoculated, virus-infected cells and not transformation of marmoset cells. S. o. oedipus showed the best serum neutralizing antibody response to BaEV and MSV(BaEV), S. fuscicollis a moderate response and C. jacchus no response.

Animals↗
PubMed1978

The "sarcoma-specific" region of Moloney murine sarcoma virus 124.

Labeled, purified 30S RNA from Moloney murine sarcoma virus was annealed to an excess of Moloney murine leukemia virus complementary DNA. Upon treatment of the resulting DNA.RNA hybrids with RNase H followed by sucrose gradient sedimentation, and undigested 18S RNA molecule was recovered. This RNA molecule was shown to represent the "sarcoma-specific" region of the virus. The unintegrated linear DNA provirus of murine sarcoma virus 124 was isolated from newly infected cells and a physical map of the sarcoma-specific region was obtained. First, unintegrated full-length linear proviral DNA molecules were cleaved by several restriction endonucleases. The reciprocal position and orientation with respect to the viral RNA of the resulting fragments were established. The location of the sarcoma-specific region was determined by competition-hybridization with 125I-labeled viral genomic RNAs and proviral DNA fragments. A 1500-base-pair fragment was obtained by cleavage with HindIII + Bgl II. This fragment mapped between 750 and 2250 base pairs from the right end of the proviral DNA (corresponding th the 3' terminus of the viral RNA) and contained the whole set of the sarcoma-specific information. This murine sarcoma virus proviral restriction fragment is approximately of the same size and map position as the isolated 18S sarcoma-specific RNA.

Animals↗
PubMed1977

Genetics of murine sarcoma virus (MSV)--induced tumors in AKR mice: Evidence that late progressing and early regressing tumors are controlled by different gents.

The genetics of late appearing MSV tumors showing a progressive growth pattern in AKR mice was investigated. The late MSV tumor response in F1 hybrids depended on the genetic background of the non-AKR parent. Within the 4-month observation period following virus injection, (CBA X AKR) F1, (DBA/2 X AKR)F1, and (NIH X AKR)F1 developed progressing MSV tumors, which exhibited latency and growth behavior comparable to that seen in AKR mice, (BALB X AKR)F1, (B6 X AKR)F1, and (B10br x akr)f1 mice did not show any late MSV tumors. In contrast to early regressing M-MSV tumors, whose development is independent of Fv-1 genotype, late MSV tumor progression is largely a function of this gene, since all late tumors which appeared in (B10BR x AKR) x AKR were observed in Fv-1n homozygous mice, H-2k halotype is a further factor in the occurrence of late MSV tumors, at least in (B6 x AKR) x AKR mice. In crosses of AKR with Fv-1 compatible mice, tumor appearance was strongly associated with inheritance of AKR-Mulv, and MSV recovered from late tumors of first back-cross animals appeared to be a new pseudotype with the endogenous AKR-MuLV. It is suggested that the host genetic control in both early and late MSV tumors is exerted mainly on the helper component of the leukemia-sarcoma complex.

Animals↗