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At least 19 recordsLinked to original sources
PubMed1987

Immunization with envelope glycoprotein of an avian RNA tumor virus protects against sarcoma virus tumor induction: role of subgroup.

Avian RNA tumor virus envelope glycoprotein protects against sarcoma development by an avian sarcoma virus of the same subgroup. Avian RNA tumor viruses, members of the retrovirus family, induce various malignancies in fowl (Weiss et al. (eds.), 1982, RNA Tumor Viruses, Cold Spring Harbor, N.Y.). These viruses consist of a genomic RNA core surrounded by an envelope with embedded glycoproteins, of 85 and 37 kDa. The 85 kDa glycoprotein is antigenically specific for each subgroup as determined by neutralization. The envelope glycoprotein can be removed from the virion with retention of its antigenicity (Duesberg et al., 1970, Virology 41, 631-646). Two fractions of 4-6S and 8S, separated by sedimentation, were shown to retain antigenicity by interference of neutralization of virus by antibody. Thus, the 4-6S and 8S preparations could possibly serve as immunogens. The objective of this study was to determine if such envelope glycoprotein preparations could function as potential vaccines, and if so, whether the protection afforded would be subgroup specific.

Animals↗
PubMed1984

RNA tumor viruses, DNA tumor viruses and developmental switches: a unifying hypothesis.

It is hypothesized that oncogenic viruses (both RNA and DNA tumor viruses) use cellular differentiation switches as part of their mechanism for viral replication. Chemical or radiation-induced carcinogenesis is the result of mutations which also affect these differentiation switches and their cellular controls. A transformed cell is characterized by the uncontrolled and inappropriate expression of embryonic (developmental) sequences. Many of the oncogenic viruses, both RNA and DNA, are lineage- and stage-specific in the cells they can productively infect, in keeping with their means of replication. The interaction between virus and host cellular controls determines whether recognizable neoplasia will result from viral infection.

Animals↗
PubMed2002

Perspectives in studies of human tumor viruses.

Tumor viruses can be found in both the RNA and DNA virus kingdoms. All RNA tumor viruses belong to the retrovirus family. Directly transforming Class I RNA tumor viruses carry cellular oncogenes, picked up by accidental recombination, and usually selected for secondary modifications and high tumorigenicity by the investigator. They are not known to play any role for tumor causation in nature. Class II or chronic RNA tumor viruses do not carry cell-derived oncogenes but they often act by proviral DNA insertion into the immediate neighborhood of a cellular oncogene. Feline, murine, and avian leukemia viruses belong to this category. The human adult T-cell leukemia virus, (HTLV-1) and bovine leukemia virus (BLV) act by expanding the preneoplastic cell population and thereby provides the soil for secondary, cellular changes. The DNA tumor viruses belong to three very different categories, the papovaviruses, adenoviruses and herpesviruses. Inactivation of the Rb and the p53 pathway by the viral transforming proteins is a convergent feature of the papova- and the adenoviruses. Since all DNA tumor viruses kill their host cell following their entry into the lytic phase, transformation and tumorigenicity are entirely dependent on a non-lytic interaction. Cells transformed by DNA tumor viruses depend on the continued expression of the virally encoded oncogene. They provide thereby a convenient target for the immune surveillance of the host. Depending on the epidemiological history of the virus in relation to its natural host species, the immune surveillance of the host and the strategy of viral latency and survival can evolve into a truly symbiotic relationship, as best illustrated by the Epstein-Barr virus (EBV). Tumor development occurs only as an accident at the level of the host (immunosuppression) or the cell (specific translocations or other genetic changes). The list of human viruses presently known to cause or to contribute to tumor development comprise four DNA viruses, namely Epstein-Barr virus, certain human papilloma viruses subtypes, hepatitis B virus, and Kaposi sarcoma herpesvirus (HHV-8); and two RNA viruses, adult T-cell leukemia virus (HTLV-1) and hepatitis virus C.

Animals↗
PubMedDate not supplied

Human tumor viruses.

Tumor viruses play an important role for the development of a substantial fraction of human malignancies, including common cancers, such as carcinomas of the cervix uteri, hepatocellular carcinomas, or lymphomas. In the recent past, much progress has been made in elucidating the molecular mechanisms by which human tumor viruses contribute to cellular growth deregulation and carcinogenesis. The picture emerges that different tumor viruses target similar cellular pathways for growth deregulation but, in addition, also have unique properties contributing to oncogenesis. Malignant transformation typically requires additional genetic alterations of the host cell, to which tumor viruses can contribute by destabilizating the cellular genome.

Cell Transformation, Viral↗
PubMed1972

Comparison of the 3' termini of discrete segments of the double-stranded ribonucleic acid genomes of cytoplasmic polyhedrosis virus, wound tumor virus, and reovirus.

The 3' terminal nucleosides of the isolated components of double-stranded ribonucleic acids of reovirus, wound tumor virus, and cytoplasmic polyhedrosis virus were determined by labeling with tritiated sodium borohydride. All wound tumor virus and cytoplasmic polyhedrosis virus components appear to contain approximately equal amounts of U(OH) and C(OH) termini. Reovirus segments have essentially only C(OH) termini.

Adenosine↗
PubMed1972

Comparison of the structure and polypeptide composition of three double-stranded ribonucleic acid-containing viruses (diplornaviruses): cytoplasmic polyhedrosis virus, wound tumor virus, and reovirus.

Iodination of reovirus, cytoplasmic polyhedrosis virus (CPV), and wound tumor virus (WTV), and their respective subviral forms, followed by analysis of the labeled polypeptides by using polyacrylamide gel electrophoresis, has been used to compare the protein contents of these three diplornaviruses. This approach, when combined with electron microscopy and buoyant density determinations, appears capable of localizing individual polypeptides in some of the viral and subviral forms. CPV (p = 1.435 g/cm(3)) seems to resemble reovirus cores (p = 1.440 g/cm(3)) in both ultrastructure and polypeptide composition. CPV is composed of five polypeptides with molecular weights of about 151,000, 142,000, 130,000, 67,000, and 33,000. The polyhedral matrix, which in nature encapsulates the virions, is, in turn, composed mainly of two polypeptide species with molecular weights of about 30,000 and 20,000, and several minor proteins. The proteins of WTV consist mainly of four species of polypeptide with molecular weights of about 156,000, 122,000, 63,000, and 44,000, and several minor components. These molecular weight determinations are consistent with the hypothesis that, as has been suggested for reovirus, the viral proteins of CPV and WTV seem to be coded for by monocistronic mes senger RNA molecules transcribed from distinct segments of the double-stranded RNA viral genomes.

Centrifugation, Density Gradient↗
PubMed2003

Regulation of mouse mammary tumor virus env transcriptional activator initiated mammary tumor virus superantigen transcripts in lymphomas of SJL/J mice: role of Ikaros, demethylation, and chromatin structural change in the transcriptional activation of mammary tumor virus superantigen.

Mammary tumor virus (Mtv29)-encoded superantigen expressed by SJL/J mouse B cell lymphomas stimulates CD4+V16+ T cells and thereby acquires T cell help necessary for lymphoma growth. Mtv29 mouse mammary tumor virus env transcriptional activator (META) env-controlled Mtv29 superantigen (vSAg29) mRNA transcripts (1.8 kb) are not expressed in normal B or other somatic cells. Real-time PCR-based assays with DNA from normal SJL liver and vSAg29- lymphoma (cNJ101), digested with methylation-sensitive enzymes, showed hypermethylation at AvaI, FspI, HpaII, ThaI, and the distal HgaI sites of the META env, but vSAg29+ lymphoma cells showed significant demethylation at AvaI, HpaII, and the distal HgaI sites. The distal HgaI site that is adjacent to an Ikaros binding site is significantly demethylated in the META env DNA from primary lymphomas. Gel shift assays showed binding of Ikaros to a sequence representing this region in the META env. SJL lymphomas expressed the Ikaros isoform Ik6 that was absent in normal B cells. vSAg29+ cells exhibited increased DNaseI accessibility to chromatin at the vSAg29 initiation site. Treatment of cNJ101 cells with a demethylating agent, 5-azacytidine, and a histone deacetylase inhibitor, trichostatin A, caused hypomethylation at AvaI, HpaII, and distal HgaI sites and led to chromatin structural change at the vSAg29 initiation site, accompanied by the expression of vSAg29 transcripts. This enabled cNJ101 cells to stimulate SJL lymphoma-responsive CD4+V16+ T hybridoma cells. Thus, demethylation at the distal HgaI site of the Mtv29 META env permits vSAg29 expression, which may have an impact on the development of germinal center-derived B cell lymphomas of SJL/J mice.

Animals↗
PubMed1998

Loss of endogenous mouse mammary tumor virus superantigen increases tumor resistance.

From a cross between a tumor-susceptible mouse strain (DBA/2; D) and a tumor-resistant MHC-identical strain (B10.D2; D2) new recombinant inbred mouse strains were established over many generations of inbreeding and tumor resistance selection. Since resistance to the highly metastatic DBA/2 lymphoma variant ESb had an immunologic basis, and the two parental strains differed in endogenous viral superantigens (vSAGs), DNA of three D2 x D recombinant inbred mouse lines was typed for endogenous mouse mammary tumor viruses using mouse mammary tumor virus long terminal repeat- and env gene-specific probes. The resistant D2 x D mice were very similar to the susceptible parental strain D in their Mtv Southern blots, except for the lack of a single band corresponding to Mtv-7, the provirus coding for the strong DBA/2 superantigen Mls-1a. A backcross analysis revealed that Mtv-7-negative F2 mice were significantly more resistant than Mtv-7-positive F2 mice. When Mtv-7 was reintroduced into the resistant lines by crossing them with either CBA/J or BALB/D2.Mls-1a, the mice became again more tumor susceptible. Finally, we demonstrate the ability to transfer immunoresistance and graft-vs-leukemia reactivity from tumor-resistant to tumor-susceptible mice.

Animals↗
PubMed1985

Molecular cloning and characterization of the genome of wound tumor virus: a tumor-inducing plant reovirus.

The double-stranded RNA genome of the tumor-inducing plant pathogen, wound tumor virus, was converted to double-stranded DNA and cloned into plasmid pBR322. Multiple apparent full-length copies of 9 of the 12 wound tumor virus genome segments were identified. The entire sequence of cloned genome segment S12, the smallest of the genome segments, was determined. This genome segment was found to be 851 nucleotides in length and to possess a single long open reading frame that extends 178 codons from the first AUG triplet (residues 35-37): information sufficient to encode a protein of the size estimated for the smallest of the previously identified wound tumor virus primary gene products, Pns 12. Sequence data obtained from analysis of cloned cDNA copies of several genome segments and from direct analysis of the 3' termini of the double-stranded genome RNAs revealed that each wound tumor virus genome segment possesses the common terminal sequences: (+) 5'GGUAUU ... UGAU 3' (-) 3'CCAUAA ... ACUA 5'.

Base Sequence↗