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Query: UMLS:C1261473 (sarcoma)
 25,952 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radioimmunological techniques were applied to the quantitation of the translational products of the gag, pol, and env genes of mammalian type C viruses. Analysis of the viral proteins associated with simian sarcoma-associated virus (SSA V) and SSA V-infected cells revealed in each that the level of reverse transcriptase was less than 1% of that of the major viral structural protein, p30. The rate of intracellular degradation of reverse transcriptase in SSA V-infected cells was found to be no greater than that of several viral structural proteins, indicating that the lower levels of viral enzyme resulted from its decreased synthesis. By screening individual cells infected at limiting SSA V dilution, it was possible to isolate a clone (clone 16), which demonstrated levels of viral p12, p30, and gp70 similar to those found in wild-type SSA V-infected cells, and which released noninfectious virions in large quantity. The noninfectious virions and clone 16 cells were shown to lack immunologically or enzymologically detectable reverse transcriptase. With serial passage of clone 16 cells, reverse transcriptase activity became spontaneously detectable in tissue culture fluids, concomitant with the appearance of infectious virus. The reverse transcriptase associated with this virus was indistinguishable from SSA V polymerase, indicating that the genetic alteration restricting SSA V pol gene expression in clone 16 cells was reversible. These results further demonstrate the strict requirement of reverse transcriptase for establishment of type C virus infection. Possible mechanisms to account for the patterns of type C viral gene expression detected in SSA V-infected cells are discussed.
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PMID:Differential synthesis of mammalian type C viral gene products in infected cells. 7 58

The DNA of normal chicken embryos contains sequences related to the avian leukosis-sarcoma viruses. RNA-dependent DNA polymerase of these viruses is encoded by a genetic element known as the pol gene. The nature of the endogenous virus pol gene in chicken cells was investigated by testing its ability to participate in genetic recombination. Rous-associated virus-60-type recombinant viruses isolated after infection of chicken cells with strains tsLA337PR-B or tsNY21SR-A, both of which produce a temperature-sensitive DNA polymerase, also possessed the temperature-sensitive lesion. These results are consistent with the hypothesis that the endogenous viral information used for the generation of Rous-associated virus-60 is deficient in at least part of the pol gene and that the defect includes that portion represented by the lesions in NY21 and LA337. The frequency of polymerase-negative BH-Rous sarcoma virus alpha formation was not affected by the levels of endogenous viral expression, which suggests that the alpha defect is not derived from the endogenous pol gene.
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PMID:Formation of Rous associated virus-60: origin of the polymerase gene. 8 20

Three factor crosses were performed between Rouse sarcoma virus mutants with temperature-sensitive markers in the pol and src genes and host range markers in the env gene. A number of recombinant viruses appeared to segregate from virus particles which were heterozygous for all three genes under study. The frequency of various recombinant genotypes in the progeny was consistent with there being no greater linkage between the neighbouring gene pairs of pol and env and env and src than between the more distant pol and src. The significance of these results to proposed mechanisms of avian retrovirus recombination is discussed.
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PMID:Genetic recombination in Rous sarcoma virus: the genesis of recombinants and lack of evidence for linkage between pol, env and src genes in three factor crosses. 9 Jan 14

A procedure has been developed to map the genetic elements of avian tumor virus RNA, which has a molecular weight of about 3 X 10(6) daltons and a poly(A) sequence at the 3' end. For this purpose, about 30 RNase T1-resistant oligonucleotides were ordered relative to the 3'-poly(A) terminus of the RNA, to construct an oligonucleotide map of viral RNAs. A cluster of seven envelope gene (env)-specific oligonucleotides, identified by their absence from the otherwise very similar oligonucleotide map of an envelope-defective deletion mutant (which lacks the major viral glycoprotein), mapped at a distance of 0.9 to 1.6 X 10(6) daltons from the poly(A) end of sarcoma virus RNA. A cluster of three sarcoma gene (src)-specific oligonucleotides, identified by their absence from the otherwise nearly identical oligonucleotide map of a transformation-defective deletion mutant mapped at a distance of 0.2 to 0.6 X 10(6) daltons from the poly(A) end of sarcoma virus RNA. The oligonucleotide maps of sarcoma viruses and of related deletion mutants were the same from the poly(A) end up to 0.2 X 10(6) daltons and included one terminal oligonucleotide, termed C, which is found in all avian tumor viruses tested so far. Preliminary mapping experiments ordering the src-specific and env-specific oligonucleotides of recombinants, selected for sarcoma and envelope genes of different parents, agree with those obtained by comparing maps of wild type viruses and deletion mutants. A partial genetic map consistent with these results suggests that the src gene maps between the env gene and the 3'-poly(A) end of viral RNA. This map reads: poly(A)-src-env-(pol, gag).
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PMID:Sequences and functions of Rous sarcoma virus RNA. 18 29

We have used mapping of large T1 oligonucleotides to examine the genome of Rous-associated virus-O (RAV-O), an endogenous virus of chickens, and to compare it with that of Prague strain Rous sarcoma virus, subgroup B, (Pr-RSV-B), an exogenous sarcoma virus. To extend the sensitivity of such comparisons, we have developed a system of nucleic acid hybridization and hybridization-competition combined with fingerprinting. This method allows us to estimate the relative degree of relatedness of various portions of the viral genomes. From the results of this study, we have concluded that the genomes of Pr-RSV-B and RAV-O are related in the following way. The 5'-terminal half of the genomes (corresponding to the gag and pol regions) is virtually identical, with only scattered single nucleotide differences. This region is followed by a region comprising 25 to 30% of the genome (the env region) which contains substantial nucleotide sequence differences, most or all of which are due to single base changes. The env-coding region can be further subdivided into three regions: a more variable region probably containing sequences coding for subgroup specificity, flanked by relatively common sequences on each side. To the 3' side of the env region, the RAV-O genome contains a very short sequence not found in Pr-RSV-B, whereas the Pr-RSV-B genome contains a much longer unrelated sequence. The central portion of this sequence comprises the src gene as defined by transformation-defective mutants. Particularly striking is the absence, in the RAV-O genome, of any nucleotide sequence related to the "c region" found very near the 3' end of all exogenous tumor viruses. Both the Pr-RSV-B and RAV-O genomes contain the identical terminally redundant sequence of 21 nucleotides near each end of the genome.
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PMID:Nucleotide sequence relationships between the genomes of an endogenous and an exogenous avian tumor virus. 21 88

The lymphoproliferative disease virus of turkeys (LPDV) is the etiological agent of a rapidly developing lymphoproliferative process in turkeys. To better understand the genetic relationships of LPDV to other retroviruses we determined the nucleotide sequence of its pol gene. Comparative computer analyses of the deduced amino acid sequences of the reverse transcriptase and integrase domains within pol established that LPDV represents a distinct class of avian retroviruses that is most closely related to the avian leukemia-sarcoma viruses.
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PMID:The lymphoproliferative disease virus of turkeys represents a distinct class of avian type-C retrovirus. 128 41

We have developed sets of degenerate oligonucleotides designed to detect pol gene sequences from any member of the lentivirus subfamily when used as primers in amplification techniques such as the polymerase chain reaction (PCR). This pan-lentivirus-specific primer set (PLSPS) consists of primers, LV1, LV2, and LV3, based on conserved regions common to lentiviruses only. Our protocol is based on primary amplification with LV1 and LV2 followed by secondary amplification with a nested primer set based on the YM/VDD motif found in all reverse transcriptases (or "DDMY," in the opposite direction), and LV3, a block of lentivirus homology nested just downstream of LV1. PLSPS-PCR analysis of DNA from cells infected with HIV-1, HIV-2, SIVmac239, BIV, visna, EIAV, CAEV, OPPV, or FIV resulted in the amplification of appropriately sized products. Sequence analysis of the LV1/2 products, cloned into pBluescript (pBS), indicated that at least 20% (most often, > 80%) contained the predicted lentivirus pol sequence. Greater than 95% of the LV3/DDMY products contained the expected lentiviral sequences. Using the PLSPS, lentivirus pol sequences could typically be detected at levels of one copy in 2 x 10(6) cells after secondary amplification. No specific lentiviral PCR products were detected in DNA from uninfected human or mouse monocytes, feline or bovine leukocytes, mouse, rat or human fibroblast cell lines, chicken embryo fibroblasts, Tahr lung cells, or cell lines infected with the following retroviruses which are not lentiviruses: Rous sarcoma virus, Moloney leukemia virus or Kirsten sarcoma virus, mouse mammary tumor virus, human T-cell lymphotropic virus I, and feline leukemia virus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Identification and evaluation of new primer sets for the detection of lentivirus proviral DNA. 133 58

We have found human DNA to contain a number of sequences related to simian sarcoma associated virus (SSAV). One of these sequences was isolated from a human genomic library. The molecular clone, termed S71, contains regions homologous to SSAV gag and pol fragments and SSAV LTR. Furthermore, hybridization experiments and DNA sequencing revealed distinct homologies to the reverse transcriptase coding region of several other retroviruses including baboon endogenous virus (BaEV) and murine leukemia viruses (MuLV) as well as retrovirus-like elements. Some sequence homology was also found with the C-type retrovirus-related multicopy human clone 4-1. S71 is present in only one copy per human genome equivalent and exhibits an EcoRI restriction fragment length polymorphism.
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PMID:Isolation of an SSAV-related endogenous sequence from human DNA. 243 42

The Harvey murine sarcoma virus genome contains two rat-derived sets of genetic information recombined with the Moloney mouse leukemia virus. The rat sequences represent a ras oncogene and a rat VL30 element. The VL30 sequences have several discrete regions of similarity with retroviral sequences which were detected by searching a protein database for similarities with predicted polypeptide sequences from the VL30 regions. On the 5' side, the most similar sequences were those of feline sarcoma viruses; on the 3' side, murine leukemia viruses were the most similar. Some of the regions of similarity could also be detected directly by searching a nucleic acid sequence database with the viral DNA sequences. The most extensive region of similarity was that which corresponded to the endonuclease in the pol gene of a murine leukemia virus. The majority of the rat-derived sequences present in the Harvey sarcoma virus genome can now be attributed exclusively to ras or retrovirus- or retrotransposon-related sequences.
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PMID:Harvey sarcoma virus genome contains no extensive sequences unrelated to those of other retroviruses except ras. 284 4

The RNA expression of a series of replication-defective recovered avian sarcoma viruses (rASVs) were studied. Abnormal-sized viral RNAs, both larger and smaller than the genome, were observed in the nonproducer cells infected with rASVs containing env and pol deletions. Each nonproducer clone contained a single provirus integrated at a unique site and expressed a unique RNA pattern. Upon rescuing of the sarcoma virus with a helper virus and subsequent cloning, the RNA pattern of individual nonproducer clones again displayed variation according to the integration sites. This was not seen in nondefective rASV or in rASVs containing only an env deletion. The aberrant RNA expression did not result from the lack of reverse transcriptase activity per se, since neither nonconditional nor temperature-sensitive mutants of RSV expressed abnormal viral RNAs in the absence of a functional reverse transcriptase. The abnormal RNA patterns could not be corrected in trans by helper virus functions. The unusual-sized RNAs in env- pol- rASV-infected cells are not due to splicing to alternative acceptor sites for src mRNA because there are no extra viral sequences between the 5' leader and the src sequences; instead, they are due to the presence of extra sequences, most likely of cellular origin, at the 3' ends of the viral RNAs. Based upon the extent of deletions in the viral genomes, the data suggest that deletion in the 3' pol region of those rASVs results in a cis effect on the transcription and processing of the 3' ends of viral RNAs. The unusual-sized viral RNAs are most likely due to read-through transcription from the right-hand terminus of provirus into downstream cellular sequences, followed by cleavage and polyadenylation at multiple sites of the 3' region of the RNA transcripts. The extent of read-through transcription appears to depend on the chromosomal location of the provirus.
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PMID:Deletion in the 3' pol sequence correlates with aberration of RNA expression in certain replication-defective avian sarcoma viruses. 298 7


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