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At least 19 recordsLinked to original sources
PubMed1978

Characterization of the env gene in avian oncoviruses by heteroduplex mapping.

The genome of ring-necked pheasant virus, an avian oncovirus, is largely homologous to the genomes of chicken oncoviruses except for a specific nonhomology in env, the gene coding for the surface glycoprotein of the virion (J. Tal, D. J. Fujita, S. Kawai, H. E. Varmus, and J. M. Bishop, J. Virol. 21:497--505, 1977). We have used this nonhomology between ring-necked pheasant virus and chicken oncoviruses in electron microscopic studies of heteroduplex molecules. The env-specific region of nonhomology is 1.5 to 1.7 kilobases in length. Its 3' boundary is located 0.6 to 0.7 kilobases from the 3' end of the genome in transformation-defective viruses and 2.5 kilobases from the 3' end in nondefective avian sarcoma viruses. Comparison of several strains of avian oncoviruses shows that the 3' half of this env region is conserved, while the 5' half is more diverged. A small area at the very 3' end of env also shows divergence between different avian oncoviruses. We found no evidence for the presence of a previously unrecognized gene between env and src. An electrophoretic comparison of the glycoproteins from various avian oncoviruses shows that those of ring-necked pheasant virus and Chinese quail virus differ in molecular weight from the glycoproteins of the chicken oncoviruses.

Alpharetrovirus↗
PubMed1979

A new virion precipitation test for oncovirus envelope antigens which detects common antigenic determinants in mammalian type-C viruses and Mason-Pfizer monkey virus.

A method for the study of oncovirus envelope antigens was developed, bases on the precipitation of intact virions by a double antibody technique. The amount of precipitated virus was then measured as reverse transcriptase activity. The method was designated the virion precipitation test (VPT). It has been used for titration of antibodies to envelope antigens of oncoviruses. The study of envelop antigens of 11 different oncoviruses permitted their differentiation into the following groups: (1) murine type-C viruses: (2) feline type-C viruses; (3) simian type-C viruses; (4) the RD-114/BEV group; (5) Mason-Pfizer monkey virus (M-PMV); (6) bovine leukemia virus; (7) avian type-C viruses; (8) mouse mammary tumor virus. No common antigenic determinants were detected in the last three groups. Mammalian type-C viruses (RD-114, NIH-MuLV, G-MuLV) had common antigenic determinants in the envelope, as demonstrated with an anti-RD-114 serum. Mammalian type-C viruses also shared antigenic determinants with M-PMV. The relationship of type-C viruses to M-PMV decreased in the following order: RD-114--NIH-MuLV--G-MuLV. It was also shown that the endogenous xenotropic feline RD-114 virus was more closely related to xenotropic NIH-MuLV than to ecotropic G-MuLV. The nature of the common antigenic determinants, as demonstrated by VPT on the surface of mammalian type-C viruses and M-PMV, and their significance for the concept of oncovirus evolution are discussed.

Animals↗
PubMed1978

Polypeptide maps of cells infected with murine type C leukemia or sarcoma oncovirus.

The polypeptide composition of murine fibroblast cells and the effect of infection by RNA sarcoma and leukemia viruses were analyzed by two-dimensional gel electrophoresis and tryptic peptide mapping. The polypeptide maps of NIH Swiss mouse embryo fibroblasts (NIH/3T3) and BALB/c mouse embryo fibroblasts (BALB/3T3) were very similar except for two major polypeptides of about 65,000 and 75,000 daltons which were not detected in BALB/3T3 cells. NIH/3T3 cells infected with either Rauscher or Gross oncoviruses and outbred Swiss mouse embryo fibroblasts (3T3 FL) showed two major polypeptrides of about 73,000 and 80,000 daltons not found in uninfected NIH/3T3 cells. The 3T3 FL cells, although uninfected, were also found to contain a high concentration of envelope glycoprotein of an endogenous oncovirus. 3T3 FL cells transformed by Moloney sarcoma virus showed changes in many polypeptides, including several major components: the disappearance or modification of a component of 60,000 daltons, an increased concentration and shift in pl of a glycoprotein of 48,000 daltons, and the apparent loss of several smaller polypeptides. None of the major changes of the transformed cells were associated with cell surface proteins labeled by lactoperoxidase-catalyzed iodination.

AKR murine leukemia virus↗
PubMed1978

Immunity to antigens associated with primate C-type oncoviruses in pregnant women.

Cell-mediated and humoral immune responses against antigens associated with primate C-type oncoviruses were evaluated in humans by microcytotoxicity and radioimmunoprecipitation assays. Five of six women tested sequentially during pregnancy developed selective cell-mediated reactivity against baboon endogenous virus (BEV)--infected human fibroblasts. Responsiveness peaked during the second and third trimesters and corresponded temporally with elevated antibody levels to BEV antigens. Similar cell-mediated reactivity was not observed in nonpregnant individuals. Selective cell-mediated reactivity directed against cells infected with the simian sarcoma virus-simian sarcoma associated virus complex (SSV--SSAV) was observed in four of 20 healthy adults (three of 14 nonpregnant, one of six pregnant). These observations suggest that cell-mediated reactivity against primate C-type oncoviruses is occasionally detected in healthy nonpregnant adults, but that during pregnancy both cell-mediated and humoral reactivity against BEV may become selectively expressed.

Animals↗
PubMed1977

Size and genetic content of viral RNAs in avian oncovirus-infected cells.

Viral complementary DNA (cDNA) sequences corresponding to the gag, pol, env, src, and c regions of the Rous sarcoma virus genome were selected by hybridizing viral cDNA to RNA from viruses that lack the env or src gene or to polyadenylic acid [poly(A)]-containing RNA fragments of different lengths and isolating either hybridized or unhybridized DNA. The specificities, genetic complexities, and map locations of the selected cDNA's were shown to be in good agreement with the size and map locations of the corresponding viral genes. Analyses of virus-specific RNA, using the specific cDNA's as molecular probes, demonstrated that oncovirus-infected cells contained genome-length (30-40S) RNA plus either one or two species of subgenome-length viral RNA. The size and genetic content of these RNAs varied, depending on the genetic makeup of the infecting virus, but in each case the smaller RNAs contained only sequences located near the 3' end of the viral genome. Three RNA species were detected in Schmidt-Ruppin Rous sarcoma virus-infected cells: 39S (genome-length) RNA; 28S RNA, with an apparent sequence of env-src-c-poly(A); and 21S RNA, with an apparent sequence of src-c-poly(A). Cells infected with the Bryan high-titer strain of Rous sarcoma virus, which lacks the env gene, contained genome-length (35S) RNA and 21S src-specific RNA, but not the 28S RNA species. Leukosis virus-infected cells contained two detectable RNA species: 35S (genome-length) RNA and 21S RNA, with apparent sequence env-c-poly(A). Since gag and pol sequences were detected only in genome-length RNAs, it seems likely that the full-length transcripts function as mRNA for these two genes. The 28S and 21S RNAs could be the active messengers for the env and src genes. Analyses of sequence homologies among nucleic acids of different avian oncoviruses demonstrated substantial similarities within most of the genetic regions of these viruses. However, the "common" region of Rous-associated virus-0, an endogenous virus, was found to differ significantly from that of the other viruses tested.

Animals↗
PubMed1977

Structural protein markers in the avian oncoviruses.

The proteins of purified avian oncoviruses were analyzed by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis and isoelectric focusing. Certain members of the avian leukosis-sarcoma viruses (ALSV) had group-specific antigens with altered electrophoretic properties. (i) The p27 protein of Rous-associated virus 0 (RAV-0) had a lower electrophoretic mobility in SDS gels and a lower isoelectric point than the p27 of other ALSV. (ii) The p19 proteins of RAV-1, RAV-2, and the Bryan high-titer strain of Rous sarcoma virus had higher mobilities in SDS gels than did the corresponding protein of other viruses. This altered electrophoretic mobility was correlated with specific differences in the tryptic peptides of radioiodinated p19s. (iii) The p15 protein of RAV-7 had a lower mobility in SDS gels than did the p15 of other ALSV. These markers were used in a study of the structural proteins of subgroup E RAV-60 produced after infection of chicken embryo cells by exogenous ALSV. Although exogenous group-specific protein markers could often be identified in the subgroup E isolates, one RAV-60 had a p27 that comigrated with the p27 of RAV-0. The p19s of two other RAV-60 isolates had electrophoretic properties that were different than those of p19s from either RAV-0 or the exogenous viruses. These results support the hypothesis that RAV-60 is generated by recombination between endogenous and exogenous oncoviruses and indicate that at least the p27 encoded by RAV-0 is closely related to a protein specified by endogenous viral information in chicken cells.

Autoradiography↗
PubMed1978

Type-C oncovirus isolate from human leukemic bone marrow: further in vitro and in vivo characterization.

Rabbit corneal cells transformed by a putative human type-C helper virus pseudotype of the mouse sarcoma virus produce large amounts of transforming and non-transforming viruses. The virions are antigenically related to the woolly monkey (simian) sarcoma-leukemia type-C oncovirus. Typical sarcoma virus lesions developed in newborn rats injected with virus-producing rabbit cells. Cells producing only the putative type-C helper viruses as a result of exposure to a high dilution of transforming virus stock induce lymphosarcomas after inoculation into newborn rats.

Animals↗
PubMed1978

The biosynthesis of oncovirus proteins.

The patterns of oncovirus protein biosynthesis are essentially similar for avian and mammalian viruses. In each case the four major internal structural proteins are synthesized as a precursor polypeptide of about 75 000 daltons, the product of the gag gene. Translation occurs on genome-sized mRNA. This polyprotein is cleaved in a series of steps to give the mature proteins. The mechanism and localization of cleavage have not yet been clarified. Viral reverse transcriptase, the product of the pol gene, also is translated on genome-sized mRNA as a precursor, which is a "read-through" product of the neighbouring gag gene. The two major envelope proteins are translated as a glycosylated precursor of apparent molecular weight about 90 000 from the env gene located on a sub-genomic RNA species. The precursor is transported to the plasma membrane where it may mark the site of virus budding. It is cleaved in transport or on the membrane, but the resulting two mature envelope proteins remain tied by disulfide bonds. Sarc, the protein product of the src gene that is responsible for transformation, is translated from a different viral mRNA than the structural proteins. Sarc has not been definitively characterized in any system.

Alpharetrovirus↗
PubMed1979

Phenotypic mixing between two primate oncoviruses.

Phenotypic mixing between the primate oncoviruses HL23V and BEV has been demonstrated to occur in doubly-infected bat lung (Tb) cells with the production of HL23V(BEV) pseudotype virus. The presence of the HL23V(BEV) pseudotype permitted the host range for replication of HL23V to be extended to murine cells previously 'resistant' to HL23V replication due to a block at the level of virus penetration. Expression of BEV genetic information was observed in doubly-infected rat cells and also in mouse and rat MSV-transformed non-producer cell lines co-cultivated with BEV-producing Tb cells. No evidence for genetic recombination between these viruses could be demonstrated.

Animals↗
PubMed1979

A marsupial oncovirus?

A virus-like particle was observed in two continuous cell lines derived from the marsupial Sminthopsis crassicaudata (Fat-tailed Dunnart). The development of the particle was similar to the development of D-type oncoviruses. Initially, a crescentof nucleoid material was observed near the nucleus in the region of the Golgi apparatus. This crescent developed into a doughnut-shaped-A-type particle which migrated through the cytoplasm towards the cell membrane where it budded either into a smooth membrane cytoplasmic vacuole or from the cell membrane. Only enveloped A-type particles were observed; no mature B-type, C-type or D-type particles were detected.

Animals↗
PubMed1979

Persistence of avian oncoviruses in chicken macrophages.

Inoculation of avian oncoviruses into 1- to 2-month old chickens led to a rapid production of antiviral humoral antibodies. Under these conditions it was found that avian leukosis viruses are sequestered in macrophages of peripheral blood, in which they can persist for a long period of time (up to about 3 years). In contrast, avian sarcoma viruses were never found in macrophages from chickens during the progression of sarcomas or after regression of the tumors.

Alpharetrovirus↗
PubMed1978

Stoichiometry and specificity of binding of Rauscher oncovirus 10,000-dalton (p10) structural protein to nucleic acids.

A structural protein of Rauscher oncovirus of about 8,000 to 10,000 daltons (p10), encoded by the gag gene, has been purified in high yield to apparent homogeneity by a simple three-step procedure. The purified protein was highly basic, with an isoelectric point of more than 9.0, and its immunological antigenicity was chiefly group specific. A distinctive property of the protein was the binding to nucleic acids. The stoichiometry of p10 binding to Rauscher virus RNA was analyzed using both 125I-labeled p10 and 3H-labeled RNA. The protein-RNA complex, cross-linked by formaldehyde, was separated from free RNA and free protein by velocity sedimentation and density gradient centrifugation. A maximum of about 140 mol of p10 was bound per mol of 35S RNA, or about one molecule of p10 per 70 nucleotides. This protein-RNA complex banded at a density of about 1.55 g/ml. The number of nucleic acid sites bound and the affinity of p10 binding differed significantly among the other polynucleotides tested. The protein bound to both RNA and DNA with a preference for single-stranded molecules. Rauscher virus RNA and single-stranded phage fd DNA contained the highest number of binding sites. Binding to fd DNA was saturated with about 30 mol of p10 per mol of fd DNA, an average of about one p10 molecule per 180 nucleotides. The apparent binding constant was 7.3 X 10(7) M(-1). The properties of the p10 place it in a category with other nucleic acid binding proteins that achieve a greater binding density on single-stranded than on double-stranded molecules and appear to act by facilitating changes in polynucleotide conformation.

Binding Sites↗
PubMed1979

Tryptic peptide analysis of avian oncovirus gag and pol gene products.

Radiolabeled tryptic peptides of the gag and pol gene products of avian oncoviruses were examined. This analysis included Rous-associated virus 2 structural proteins and the Pr76gag and P180gag-pol proteins in Rous-associated virus 2-infected chicken embryo cells. The methionine- and cysteine-containing tryptic peptides of virion internal structural proteins were present in both Pr76gag and P180gag-pol, suggesting that there was no loss of gag gene-coding sequences during the generation of P180gag-pol. No overlap of gag and pol gene structural information was detected. Analysis of intermediates in the processing of Pr76gag and translation inhibition mapping with pactamycin yielded the following order of structural proteins within the Rous-associated virus 2 Pr76gag precursor: NH2-p19-p12-p27-p15-COOH. The gag and pol sequences missing in the endogenous gsmp120 protein of uninfected gs+ chicken cells were identified by comparison with those of Rous-associated virus 2 P180gag-pol.

Animals↗
PubMed1979

Interactions between cellular membrane receptors and oncovirus envelope glycoprotein: influence of enzymes and protein-modifying reagents on receptors.

Binding of purified envelope glycoprotein (gp69/71) of Rauscher murine type C oncovirus to cellular membrane receptors has been analyzed with reaction systems using intact cells or membranes of disrupted cells. The reaction was highly specific; only cells permissive to infection by Rauscher virus bound the 125I-labeled viral glycoprotein. The specificity of binding was also demonstrated with respect to virus interference; cells productively infected with murine ecotropic type C virus failed to bind the virus envelope glycoprotein, whereas permissive cells infected with murine xenotropic virus continued to bind the Rauscher ecotropic virus glycoprotein. The reaction required the presence of Ca2+ or Mn2+ and was rapid and reversible. Studies of the enzymatic digestion of membranes suggested that the receptor is a protein which requires lipid either for its activity or for the integrity in the membrane. Receptor binding was greatly reduced by modification of histidine, tyrosine, and tryptophan residues.

2-Hydroxy-5-nitrobenzyl Bromide↗
PubMed2025

Comprehensive Analysis of Clinical and Molecular Features in Cancer Patients Associated With Major Human Oncoviruses.

Viral infections contribute to a higher incidence of cancer than any other individual risk factor. This study aimed to compare the clinical and molecular features of four viral-associated cancers: stomach adenocarcinoma (STAD), head and neck squamous cell carcinoma (HNSC), liver hepatocellular carcinoma (LIHC), and cervical squamous cell carcinoma (CESC). Patients were categorized based on viral infection status, as provided in the clinical data, into virus-associated and non-virus-associated groups, followed by a comprehensive comparison of clinical and molecular features. Our analysis disclosed that viral infections confer unique clinical and molecular signatures to their associated tumors. Specifically, human papillomavirus-associated (HPV+) HNSC and hepatitis B virus-associated (HBV+) LIHC patients were predominantly male, younger, and exhibited better clinical prognoses. Virus-associated tumors displayed enhanced immune microenvironments and high DNA damage response scores, while non-virus-associated tumors were enriched in stromal signatures. HPV+ HNSC and Epstein-Barr virus-associated (EBV+) STAD showed similarities across multi-omics features, including better responses to immunotherapy, lower TP53 mutation rates, tumor mutation burden (TMB), and copy number alteration (CNA). Conversely, HBV+, Hepatitis C virus-associated (HCV+) LIHCs and HPV+ CESC were more genomically unstable due to high TP53 mutation rates, TMB, and CNA. At the protein level, Caspase-7 and Syk were upregulated in HPV+ HNSC and EBV+ STAD, and positively correlated with the enrichment levels of CD8 + T cell, PD-L1, and cytolytic activity. Patient stratification based on infection status has significant clinical implications, particularly for patient prognosis and drug response.

Humans↗
PubMed2025

Defective but tumorigenic: the evolutionary and functional roles of mutated oncoviruses.

Human oncogenic viruses contribute significantly to the global health burden and include seven types: Epstein-Barr virus, hepatitis B virus, human T-cell leukemia virus type 1, human papillomavirus, hepatitis C virus, Kaposi's sarcoma-associated herpesvirus, and Merkel cell polyomavirus. While the roles of latent or integrated viral genomes in cancer have been documented, emerging evidence highlights the contribution of defective viruses-those carrying intragenic deletions or loss-of-function mutations-in promoting viral oncogenesis. These altered genomes often lack genes essential for lytic replication or immune recognition, which enhances their persistence and immune evasion. In virus-associated diseases, specific patterns of gene retention and deletion suggest that host-driven selective pressures drive the emergence of these altered genomes. This review examines the generation, prevalence, and functional impact of these viruses, reframing them as active participants in disease development and progression. Recognizing their role offers new insights into viral tumor evolution and creates opportunities for applications in viral diagnostics and targeted intervention strategies.

Humans↗