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At least 19 recordsLinked to original sources
PubMed1975

Differential expression of helper viral structural polypeptides in cells transformed by clonal isolates of woolly monkey sarcoma virus.

Cell lines transformed by woolly monkey sarcoma virus (WSV) in the absence of infectious virus production were analyzed for the expression of woolly monkey helper viral p30, p12, and gp70 antigens. Several lines produced high levels of both p30 and p12, whereas gp70 was not detectable. One transformed clone expressed only p12, and in another cell line, none of the helper viral antigens were detected. The properties of each sarcoma virus bred true upon transmission, indicating that each variant represents a distinct genotype. The different cell lines were examined with respect to properties characteristic of the transformed state. The in vitro growth properties and oncogenicity of each WSV-transformed clone were indistinguishable, indicating that transformation by WSV occurs independently of the expression of at least three helper viral polypeptides.

Animals↗
PubMed1974

Surface antigens of mammalian sarcoma virus-transformed nonproducer cells.

In vitro, clonal BALB/3T3 mouse cells were transformed into nonproductive sarcoma cells by Kirsten murine sarcoma virus. The resulting cells are called K-BALB. Similarly, the Kirsten sarcoma virus and woolly monkey sarcoma virus transformed normal rat embryonic kidney (NRK) cells to nonproductive sarcoma cells K-NRK and W-NRK, respectively. The presence of sarcoma cell surface antigen (SCSA) on these three different cell lines has been examined by immunoelectron microscopy using the rabbit anti-K-BALB, anti-K-NRK, and anti-W-NRK sera preabsorbed with normal embryonic rat cells, NRK cells, and BALB/3T3 cells. Four different specific sarcoma cell surface antigens have been demonstrated: SCSAa, an antigen specific to the surface of W-NRK cells; SCSAb, a surface antigen common to K-NRK and W-NRK cells; SCSAc, a surface antigen common to K-BALB and W-NRK cells; and SCSAd, a surface antigen broadly reactive with the rabbit antisera to W-NRK, K-NRK, and K-BALB.

Animals↗
PubMed1975

Type C RNA tumor virus isolated from cultured human acute myelogenous leukemia cells.

Previously, type C RNA tumor virus-related components have been described in blood leukocytes from patients with acute myelogenous leukemia. These components, for example, reverse transcriptase, have been shown to be most closely related to those from two oncogenic subhuman primate type C viruses (woolly monkey sarcoma virus and gibbon ape leukemia virus). Now, we report the continuous production of budding type C viruses with the same characteristic reverse transcriptase by three separate culturings of leukocytes from a single bleeding from a patient with acute myelogenous leukemia. These isolations were made possible by the discovery of a source of conditioned media which sustains exponential growth of human myelogenous leukemia cells in liquid suspension culture.

Cell Differentiation↗
PubMed1976

Natural antibodies in sera from healthy humans to antigens on surfaces of type C RNA viruses and cells from primates.

Sera from healthy humans contained naturally occurring antibody against group- or subgroup-specific antigen on the envelope of the following type C viruses isolated from primates: gibbon ape leukemia virus, simian (woolly monkey) sarcoma virus, baboon endogenous type C virus, and putative human type C viruses [HL23V isolated from blood cells of a patient with acute myelogenous leukemia (HL23) and HEL-12V from human embryonic diploid cells (CIH-32)]. Two sera also reacted with C57BL/6 mouse leukemia induced by Friend virus. These results were obtained by indirect immunoelectron microscopy with various virus-producing cells and by absorption tests using as targets gibbon lymphosarcoma cells that release gibbon ape leukemia virus. In a previous report, the presence of natural antibody in sera from healthy gibbon apes was demonstrated. When the specificities of the human and gibbon natural antibodies were compared, the human natural antibody reacted with two nonproducing culture cell lines of human lymphocytic leukemia (CEM-A and MOLT) and with human embryonic diploid (CIH-1(V-) cells [which became type C virus-producing CIH-32(V+) cells after many passages], but did not react with normal gibbon spleen monolayer cells. In contrast, gibbon natural antibody showed no reaction with CEM-A, MOLT, and CIH-1(V-) cells but reacted with gibbon spleen monolayer cells. Neither human nor gibbon natural antibody that was reactive with gibbon ape leukemia virus crossreacted with feline leukemia virus and mouse wild-type AKR leukemia virus. The gibbon lymphosarcoma cells releasing gibbon ape leukemia virus were used in a screening study of sera from healthy humans. Out of 72 sera screened by indirect immunoelectron microscopy using this system, 55 were positive (76%), i.e., 26 out of 35 males (74%) and 29 out of 37 females (78%). The highest incidence of antibody production was in 1- to 10-year-olds and 31- to 40-year-olds, with the adults exhibiting higher levels. Differences in incidence of natural antibody were not found to be sex-linked. These findings suggest that type C RNA viruses related to the gibbon ape leukemia virus and simian (woolly monkey) sarcoma virus family as well as the baboon endogenous type C virus family may be widespread in humans.

Animals↗
PubMed1986

Efficient reversion of simian sarcoma virus-transformation and inhibition of growth factor-induced mitogenesis by suramin.

Simian sarcoma virus, an acutely transforming primate retrovirus with capacity to induce gliomas and sarcomas in experimental animals, has acquired its transforming properties by transducing the cellular gene sequences that encode one of the constituent chains of platelet-derived growth factor. Suramin, a drug used in the treatment of trypanosomiasis and onchocerciasis, has previously been reported to inhibit the interaction of platelet-derived growth factor with its cell surface receptor. We show here that suramin efficiently reverts the simian sarcoma virus-induced transformed phenotype in human and rat fibroblasts and propose that this is due to neutralization of an externalized v-sis product. Moreover, we show that suramin inhibits the action of a broad spectrum of growth factors.

Animals↗
PubMed1977

Interruption of oncornavirus replication by modified rifamycin antibiotics.

Thirteen rifamycin SV derivatives containing 3'-alkylaminomethyl substituents fail to inhibit the activities of the simian sarcoma virus Type 1 DNA polymerase, and of cellular DNA, RNA, and poly(A) polymerases prepared from NIH Swiss mouse embryos. These compounds show a range in their toxicities for NIH Swiss mouse 3T3 cells and in their capacities to inhibit production of foci of morphologically altered cells by murine sarcoma virus (MSV). Three compounds--the N-methyl-N-hydroxyethylaminomethyl, the N,N-dimethyl-aminomethyl, and the N4-methylpiperazinomethyl rifamycin derivatives--are comparable to adenine arabinoside and ribavirin in their toxicity for 3T3 cells, but these compounds show superior focus inhibition. These compounds inhibit oncornavirus production apparently by exacerbation of a delay in growth that results from infection of 3T3 cells with MSV.

Cell Survival↗
PubMed1981

Three distinct genes in human DNA related to the transforming genes of mammalian sarcoma retroviruses.

Southern blot hybridization was used to identify human and other vertebrate DNA sequences that were homologous to cloned DNA fragments containing the oncogenic nucleic acid sequences of three different type C mammalian retroviruses (simian sarcoma virus, the Snyder-Theilen strain of feline sarcoma virus, and the Harvey strain of murine sarcoma virus). Each onc gene counterpart has a single genetic locus, which probably contains non-onc intervening sequences. The human DNA sequences may represent genes important to cell growth or cell differentiation, or both. Their identification and isolation may allow elucidation of their role in these processes and in neoplasias.

Animals↗
PubMed1982

Nucleotide sequence analysis of the long terminal repeat of integrated simian sarcoma virus: evolutionary relationship with other mammalian retroviral long terminal repeats.

Nucleotide sequence analysis of the long terminal repeat (LTR) of the integrated simian sarcoma virus showed that the simian sarcoma virus LTR comprised 504 nucleotides with an inverted repeat of seven bases at its 5' and 3' termini. At the site of simian sarcoma virus integration, cellular flanking sequences adjacent to the proviral LTR contained a direct repeat of four bases. A 13-base sequence after the 5' LTR was found to be complementary to prolyl tRNA, suggesting that tRNAPro may serve as the primer for reverse transcription of simian sarcoma virus RNA. The U5 and R regions, derived respectively from the 5' end and terminally redundant sequences of the viral RNA, were found to have similar organization and sequence homology close to that of Moloney murine sarcoma virus or Moloney murine leukemia virus. These results indicate that regions within LTRs with known functionally important sequences have been most well conserved during retrovirus evolution.

Biological Evolution↗
PubMed1983

Nucleotide sequences of feline sarcoma virus long terminal repeats and 5' leaders show extensive homology to those of other mammalian retroviruses.

The nucleotide sequences of the Gardner-Arnstein feline sarcoma virus (FeSV) long terminal repeat and the adjacent leader sequences 5' to the viral gag gene were determined. These were compared with homologous portions of Synder-Theilen FeSV and with previously published sequences for Moloney murine sarcoma virus and simian sarcoma virus proviral DNA. More than 75% of the residues in the FeSV R and U5 regions were homologous to sequences within the same regions of the other viral long terminal repeats. Unexpectedly, alignment of the FeSV sequences with those of the Moloney murine sarcoma and simian sarcoma viruses showed similar extents of homology within U3. The homologous U3 regions included the inverted repeats, a single set of putative enhancer sequences, corresponding to a "72-base-pair" repeat, and sequences, including the CAT and TATA boxes, characteristic of eucaryotic promotors. The 5' leader sequences of both FeSV strains included a binding site for prolyl tRNA and a putative splice donor sequence. In addition, the FeSV leader contained a long open reading frame which was adjacent to and in phase with the ATG codon at the 5' end of the FeSV gag gene. The open reading frame could code for a signal peptide of about 7.4 kilodaltons. Our results support the concept that the virogenic portions of both FeSV and simian sarcoma virus were ancestrally derived from viruses of rodent origin, with conservation of regulatory sequences as well as the viral structural genes.

Base Sequence↗
PubMed1983

The Parodi-Irgens feline sarcoma virus and simian sarcoma virus have homologous oncogenes, but in different contexts of the viral genomes.

We have identified the oncogene and the putative transforming protein of the Parodi-Irgens feline sarcoma virus (PI-FeSV). The PI-FeSV is defective and needs a helper virus for its replication. The v-onc sequences in the PI-FeSV were found to be related to the v-sis sequences of the simian sarcoma virus (SSV). PI-FeSV nonproducer cells express two viral RNAs, a 6.8-and a 3.3-kilobase RNA. The 6.8-kilobase RNA contains gag, sis, and env sequences but lacks the pol gene. The 3.3-kilobase RNA, on the other hand, contains only env sequences. We have detected one feline leukemia virus-related protein product in these cells, namely, a 76-kilodalton protein which contains determinants of the feline leukemia virus gag proteins p15 and p30. The v-sis sequences in the PI-FeSV have been located near the 5' end of the viral genome. Taken together, these results imply that the p76 protein contains both feline leukemia virus gag and sis sequences and probably is the transforming protein of this virus. In contrast, in SSV the sis sequences are located towards the 3' end of the viral genome, and the sis protein is thought to be expressed via a subgenomic RNA. PI-FeSV and SSV therefore use different schemes to express their onc-related sequences. The v-sis sequences in the PI-FeSV contain restriction sites which reflect the different origin of the v-sis sequences in the PI-FeSV and SSV. The homologous oncogenes of the PI-FeSV and SSV thus were transduced by two different retroviruses, feline leukemia virus and the simian sarcoma-associated virus, apparently from the genomes of different species.

Base Sequence↗
PubMed1985

Safety of human blood products: inactivation of retroviruses by heat treatment at 60 degrees C.

Acquired immune deficiency syndrome (AIDS) can be transferred to patients by blood transfusions or human blood preparations, such as cryoprecipitates or factor VIII concentrates. Retroviruses have been discussed as infectious AIDS agents and more recently human T-lymphotropic retroviruses designated as HTLV type III and LAV (lymphadenopathy-associated virus) have been isolated from AIDS patients. Whether heat treatment at 60 degrees C (pasteurization) of liquid human plasma protein preparations inactivates retroviruses was therefore investigated. Pasteurization had already been included in the routine manufacturing process of human plasma protein preparations in order to guarantee safety with regard to hepatitis B. Since high titer preparations of human retroviruses were not available, heat inactivation was studied using Rous sarcoma virus added to the various plasma protein preparations tested. This retrovirus which was obtained in preparations of 6.0 log10 FFU/ml was shown to be at least as heat stable as two mammalian retroviruses studied, i.e., feline and simian sarcoma virus. In all of eight different plasma protein preparations tested, Rous sarcoma virus was completely inactivated after a heat treatment lasting no longer than 4 hr. It is thus concluded that pasteurization of liquid plasma protein preparations at 60 degrees C over a period of 10 hr must confer safety to these products with respect to AIDS, provided that the AIDS agents are retroviruses of comparable heat stability as Rous sarcoma virus and the mammalian retroviruses tested.

Acquired Immunodeficiency Syndrome↗
PubMed1978

[Characterization of the viral-type nucleotide sequences detected in the RNA of human leukaemic cells by probes of murine and simian origins (author's transl)].

Molecular hybridization techniques were used for searching nucleic acid sequences homologous to murine and simian oncornaviral genomes in the RNA of various categories of human leukaemic cells. We report attempts to characterize the sequences that were detected in defined categories of leukemias. It is shown that: i) although there is some correlation between the two probes used in our study with regard to the positivity or the negativity of the tests for the same leukaemic cases, there are also some discrepancies since some of the cases are positive with one probe and negative with the other; ii) the common sequences of the two probes when isolated, were ineffective to detect any complementary sequences in leukemic cases which were scored as positive when the entire probes were used; iii) the complementary sequences detected in three positive cases of acute myelogenous leukemias by a recycled probe are additive and therefore most probably distributed along the viral genome.

Animals↗
PubMed1985

Inhibition by retinoic acid of murine retrovirus-induced cellular transformation and tumor formation.

The effect of all-trans-retinoic acid (RA) on cellular transformation and on tumorigenicity of retrovirally transformed cells was investigated. RA treatment of NRK and NIH/3T3 cells transformed by BALB/c murine sarcoma virus (MuSV), Kirsten murine sarcoma virus (K-MuSV), and simian sarcoma virus resulted in a significant reduction in anchorage-dependent growth of only K-MuSV-transformed NRK cells. A 62% reduction in cell number was observed at 10(-5) M RA. In contrast, anchorage-independent growth induced by each of the viruses tested was suppressed by RA. Balb/cMSV3T3 cells showed the greatest level of sensitivity with a significant reduction in anchorage-independent growth occurring at 10(-9) M RA. The level of cytoplasmic retinoic acid-binding protein (CRABP) was determined in both parent and transformed cell lines. CRABP was present at a high level in all 3T3 cell types but was absent in all NRK cell lines. For testing the antineoplastic activity of RA in vivo, Balb/cMSV3T3 cells were injected intradermally into nude mice. Subsequent treatment of the tumor sites of these animals by topical application of RA resulted in a significant reduction in both tumor incidence and tumor size, confirming the in vitro results. Analysis of the level of v-onc mRNA revealed that inhibition of retroviral transformation by RA was not due to a decrease in transcription of the v-onc genes.

Animals↗