Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously described a nonconditional mutant of avian sarcoma virus (SE21Q1b) which fails to package viral RNA (Gallis et al., Virology 94:146-161, 1979; Linial et al., Cell 15:1371-1381, 1978). Quail cells transformed by SE21Q1b contain normal amounts of intracellular viral mRNA's for src, env, and gag-pol and release particles with the density of normal virus containing a typical complement of virion proteins, including reverse transcriptase. These virions are noninfectious for both chicken and quail cells and contain primarily cellular rather than viral RNA. Analysis by gel electrophoresis of the cellular DNA of quail cells transformed by SE21Q1b after restriction endonuclease digestion indicated the presence of a single provirus. The provirus was located at one site in the genome of the host cell and was flanked by the characteristic terminally repeated sequences derived from the 3' and 5' ends of viral RNA. The only defect detected in the SE21Q1b provirus was a deletion of ca. 150 base pairs of DNA somewhere between 300 and 600 bases from the left (gag-pol) end of the provirus. Analyses of the proviral DNA of cells transformed by wild-type recombinants between SE21Q1b and leukosis viruses reveal that the recombinants no longer contain this deletion. The deletion, therefore, defines a region on the viral RNA which is required for correct packaging of the virion RNA.
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PMID:Avian oncovirus mutant (SE21Q1b) deficient in genomic RNA: characterization of a deletion in the provirus. 625 70

OK10, a defective leukemia virus, is produced as a defective particle by so-called nonproducer transformed quail fibroblasts. OK10 defective viral particles contain an 8-kilobases (kb)-long genomic RNA, lack any detectable reverse transcriptase activity, and are not infectious. We studied the genetic content of OK10 RNA extracted from both virions and infected cells. As shown by RNA-cDNA hybridizations in stringent conditions, about 77% (6.4 kb) of the OK10 8.0kb RNA was related to avian leukosis viruses in the three structural genes gag, pol, and env, as well as in the c region. The remainder of the OK10 genome-encoding capacity (</=1.6 kb) was homologous to the MC29-specific transforming sequence myc(m) and therefore has been named myc(o). EcoRI restriction analysis of the OK10 integrated proviral DNA with different probes indicated the presence of only one provirus in the OK10 QB5 clone, which agreed with the gene order: 5'-gag-Deltapol-myc(o)-Deltaenv-c- 3'. Heteroduplex molecules formed between the viral OK10 8.0-kb RNA and the 6.8-kb SacI DNA fragment of the Prague A strain of Rous sarcoma virus confirmed that structure and indicated that the myc(o) sequence formed a continuous RNA stretch of 1.4 to 1.6 kb long between Deltapol and Deltaenv. We also examined the myc(o)-containing mRNA's transcribed in OK10-transformed cells. OK10-transformed quail fibroblasts (OK10 QB5) transcribed two mRNA species of 8.0 and 3.6 kb containing the myc(o) sequence. The genetic content of the 3.6-kb species made it a possible maturation product of the genome size 8-kb species by splicing out the gag and pol sequences. In OK10-transformed bone marrow cells (OK10 BM), a stable bone marrow-derived cell line producing OK10, the myc(o) sequence was found in four RNA species of 11.0, 8.0, 7.0, and 3.6 kb. Again, the genetic content of these mRNA's indicated that (i) the 3.6-kb species could be spliced out of the 8.0-kb-genome size mRNA and (ii) the 11.0-kb-long mRNA could represent a read-through of the OK10 provirus, the corresponding maturation product being, then, a 7.0-kb mRNA. The 7.0- and 3.6- kb mRNA's both contained the myc(o) sequence, but no sequences related to the gag or pol gene. In conclusion, whereas the myc sequences have been generally thought to be expressed through a gag-onc fusion protein, as for MC29 and CMII viruses, our experiments indicate that they could also be expressed as a non-gag-related product made from a subgenomic mRNA in the OK10-transformed cells.
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PMID:Subgenomic mRNA in OK10 defective leukemia virus-transformed cells. 628 57

Baboon endogenous virus (BaEV) is a type C retrovirus present in multiple proviral copies in the DNA of baboons. Although interspecies antigenic determinants present on reverse transcriptase and gag proteins are shared among all mammalian type C viruses, no nucleic acid homology between BaEV and other type C viruses (except RD-114) has been found in conventional liquid hybridization experiments. In this study, we used restriction fragments of cloned BaEV DNA immobilized on nitrocellulose to test for relatedness with [(32)P]cDNA's of various type C and type D viruses. We detected the following distant relationships previously found only through immunological and protein sequencing techniques: (i) eight type C viral cDNA's (the endogenous virus of rhesus monkeys, feline leukemia virus, simian sarcoma virus, gibbon ape leukemia virus, Rauscher murine leukemia virus, BALB-2, NZB, and RD-114) and two type D viral cDNA's (Mason-Pfizer monkey virus and squirrel monkey retrovirus) were able to hybridize with cloned BaEV DNA; (ii) the eight type C probes hybridized to restriction fragments spanning most of the BaEV genome, but only RD-114 hybridized to fragments within the 1.9 kilobases at the 3' end of the genome; (iii) the two type D probes hybridized primarily to fragments within the 1.9 kilobases at the 3' terminus and weakly or not at all elsewhere; and (iv) [(32)P]cDNA's of several other oncornaviruses (mouse mammary tumor virus, equine infectious anemia virus, bovine leukemia virus, and reticuloendotheliosis virus) exhibited no homology with BaEV DNA. DNA sequence analysis has allowed us to orient the BaEV restriction map with the genetic map at both ends of the genome. Homologies between retroviral cDNA's and BaEV clone restriction fragments could thus be related to specific BaEV genes. Whereas type C cDNA's hybridized to fragments from gag, pol, and the pol-env junction, squirrel monkey retrovirus cDNA hybridized only to a fragment coding for the p15E portion of env. Mason-Pfizer monkey virus cDNA also hybridized within the p15E region, but exhibited homology to the 3' half of gp70 as well. These results are discussed relative to previously reported antigenic relatedness of retroviral proteins. The data suggest that BaEV represents an important link in oncornavirus evolution.
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PMID:DNA sequence relationship of the baboon endogenous virus genome to the genomes of other type C and type D retroviruses. 628 72

The synthesis and processing of B77 avian sarcoma virus RNA in infected chicken embryo fibroblasts was followed in the presence and absence of cycloleucine, a competitive inhibitor of the synthesis of S-adenosylmethionine and thus an inhibitor of RNA methylations. An increase in the steady-state levels of genome-length RNA and a decrease in the steady-state levels of subgenomic RNA molecules were obtained in the S-adenosylmethionine-depleted avian sarcoma virus-infected cells after 24 h of treatment with the inhibitor. The total number of virus-specific RNA molecules per cell, however, remained relatively constant under either condition. The production of newly synthesized virus-specific RNA in cycloleucine-treated and untreated cells infected with a transformation-defective strain of B77 avian sarcoma virus was followed as a function of [(3)H]uridine labeling time. The accumulation of radioactive genome-length 8.4-kilobase (kb) RNA continued in cycloleucine-treated cells, and virus particle production proceeded at normal rates as previously shown by incorporation of labeled nucleoside precursors or amino acids. In contrast, newly synthesized 3.5-kb subgenomic mRNA, the putative mRNA for the envelope protein precursor, failed to accumulate in the treated cells. The extent of the inhibition in the appearance of the radioactive 3.5-kb RNA was correlated with the extent of the inhibition of viral genomic and cellular mRNA methylations and was a function of the cycloleucine concentration. Under conditions in which the accumulation of 3.5-kb envelope protein mRNA was blocked by the cycloleucine treatment, there were significant increases in the rate of synthesis of the polypeptide products of the genome-length RNA, the precursors to the non-glycosylated gag proteins (Pr76(gag)), and the reverse transcriptase (Pr 180(gag pol)) relative to the rate of synthesis of the envelope protein precursor (gPr 92(env)). These results suggest that there is an S-adenosylmethionine requirement for the splicing, but not for the synthesis, packaging, or messenger function, of avian retrovirus genome-length RNA. Possible reasons for this requirement are discussed.
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PMID:Accumulation of spliced avian retrovirus mRNA is inhibited in S-adenosylmethionine-depleted chicken embryo fibroblasts. 628 5

The H strain of avian erythroblastosis virus (AEV-H) was recently isolated from the liver emulsion of a chicken that suffered from erythroblastosis after being inoculated with subgroup A leukosis virus. AEV-H induced erythroblastosis or sarcoma when inoculated into chickens and transformed chick embryo fibroblasts (CEF) in vitro. Analysis of viral proteins synthesized in cells, which were named HNP, transformed by AEV-H but not producing transforming virus revealed tha the genome of AEV-H directed the synthesis of the gag gene products, Pr76gag and Pr180gag-pol, which was the precursor of active reverse transcriptase. Thus the HNP produced virions that were not infectious due to a defect of the env gene. Studies on the viral RNA showed that a 35 S RNA, estimated to be 8000 nucleotides long, was the genomic RNA of AEV-H and probably carried one transforming gene, which is most likely erbB gene. The gene organization of AEV-H was suggested to be 5'-gag-pol-onc-3'. These data imply that the single oncogene is responsible for both erythroblastosis and sarcoma.
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PMID:Newly generated avian erythroblastosis virus produces noninfectious particles lacking env-gene products. 631 Aug 84

The stabilities of B77 avian sarcoma virus intracellular RNAs were compared to the stability of the total cellular poly(A)-containing RNA by labelling infected chicken embryo fibroblasts with [3H]uridine for 15 h, adding actinomycin D (1 microgram per ml) to block further transcription of viral RNA, and selecting virus-specific RNA from the total cellular poly(A)-containing RNA at 3 hourly intervals. The three virus-specific RNA species (9.3, 3.3 and 5.4 kilobases) decayed with half-lives of 7.5, 10, and 15 h, respectively, whereas the bulk of the cellular mRNA decayed with a half-life of 13 h. To correlate these decay rates with the disappearance of mRNA activities, the actinomycin D-treated cells were pulse-labelled with [3H]leucine at 3 hourly intervals after the addition of the drug and virus-specific protein synthesis was assayed by immunoprecipitation. The mRNA activity for the precursor to the non-glycosylated viral structural proteins (Pr76gag) decayed with a half-life of approximately 6 h, whereas the mRNA activity coding for the precursor to the envelope proteins (gPr92env) decayed with a half-life of 14 h. Thus, the rate of decay of the individual mRNA species corresponded reasonably well with the decay rate for the synthesis of two of the corresponding gene products. The results indicated that the 5.4 kb env mRNA is more stable under these conditions than the 9.3 kb gag mRNA but was not significantly more stable than the bulk of the cellular mRNA. Virus particle production following the addition of actinomycin D was determined by the reverse transcriptase assay and by the incorporation of viral genomic 70S RNA into extracellular virions. Both assays yielded similar results and indicated that particle production was inhibited at a rate (t 1/2 = 4 h) somewhat faster than the decay of Pr76gag synthesis or the disappearance of 9.3 kb RNA. It was established by two independent methods (pulse and chase, and approach to isotope equilibrium), however, that the intracellular half-life of the RNA that is packaged into virions is 6 to 7 h. Thus, these results suggest that a single metabolic pool of 9.3 kb RNA exists in avian sarcoma virus-infected cells and is used both as mRNA and as genome RNA.
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PMID:Stabilities of avian sarcoma virus RNAs: comparison of subgenomic and genomic species with cellular mRNAs. 631 51

Synchronized mouse cells (JLS-V9) chronically infected with Rauscher murine leukemia virus were used to study virus production, the synthesis of gag and env precursor proteins, and the expression of env protein on the cell surface during the cell cycle. The amount of virus released into the medium by synchronized cells during a 30-min interval was determined by using the XC plaque assay and by measuring reverse transcriptase activity. The results show that virus production occurs during mitosis. Labeling of the cell surface of synchronized cells with 125I or with fluorescein-conjugated antiserum shows that the amount of gp 70env on the cell surface parallels cellular growth. Therefore, the cell cycle-dependent release of virus is not accompanied by similar variations in the amount of viral envelope protein on the cell surface. Immunoprecipitation of cells labeled with [35S]methionine, followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, was used to measure viral protein synthesis during the cell cycle. The rate of synthesis of gag precursor proteins show three maximums corresponding to the G1, middle S, and late S to G2 phases of the cell cycle. The rate of synthesis of env precursor proteins does not change, suggesting that in these cells the synthesis of these two gene products is controlled separately.
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PMID:Retrovirus gene expression during the cell cycle. I. Virus production, synthesis, and expression of viral proteins in Rauscher murine leukemia virus-infected mouse cells. 728 18

The human immunodeficiency virus type 1-specific Vpu protein is a small integral membrane phosphoprotein that induces degradation of the virus receptor CD4 in the endoplasmic reticulum and, independently, increases the release of progeny virions from infected cells. To address the importance of Vpu for virus replication in primary human cells such as peripheral blood mononuclear cells (PBMC) and monocyte-derived macrophages (MDM), we used three different sets of monocyte-tropic molecular clones of human immunodeficiency virus type 1: a primary isolate, AD8+, and two chimeric variants of the T-cell-tropic isolate NL4-3 carrying the env determinants of either AD8+ or SF162 monocyte-tropic primary isolates. Isogenic variants of these chimeric viruses were constructed to express either wild-type Vpu or various mutants of Vpu. The effects of these mutations in the vpu gene on virus particle secretion from infected MDM or PBMC were assessed by determination of the release of virion-associated reverse transcriptase into culture supernatants, Western blot (immunoblot) analysis of pelleted virions, and steady-state or pulse-chase metabolic labeling. Wild-type Vpu increased virus release four- to sixfold in MDM and two- to threefold in PBMC, while nonphosphorylated Vpu and a C-terminal truncation mutant of Vpu were partially active on virus release in primary cells. These results demonstrate that Vpu regulates virus release in primary lymphocyte and macrophage cultures in a similar manner and to a similar extent to those previously observed in HeLa cells or CD4+ T-cell lines. Thus, our findings provide evidence that Vpu functions in a variety of human cells, both primary cells and continuous cell lines, and mutations in Vpu affect its biological activity independent of the cell type and virus isolate used.
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PMID:Augmentation of virus secretion by the human immunodeficiency virus type 1 Vpu protein is cell type independent and occurs in cultured human primary macrophages and lymphocytes. 749 79

PCR amplification of baboon endogenous virus (BaEV) long terminal repeat, reverse transcriptase gene, and env fragments from 24 different species of African monkeys indicates that BaEV is less widespread than was formerly thought. Instead of being present in every species of African primates, BaEV can be found only in baboons, geladas, and mangabeys (all belonging to the Papionini tribe) and in African green monkey (Cercopithecus aethiops)subspecies. BaEV, which can be activated from baboon and gelada tissues, was most likely introduced in the germ line only recently (less than a few million years ago) and has not been inherited from a common ancestor of all extant African monkeys. Neighbor-joining and maximum-likelihood analyses of the sequences obtained showed that two distinct virus clusters can be distinguished: the first containing baboon, gelada, and African green monkey BaEV sequences and the second consisting of mandrill and mangabey BaEV sequences. This viral evolutionary tree does not follow host phylogeny, indicating the cross-species transmissions and multiple germ line fixations of the virus must have occurred in the past. BaEV sequences are found in monkeys inhabiting savannas (baboons, geladas, and African green monkeys) as well as forests (managabeys and mandrills) and cluster according to the habitats of their hosts, providing evidence for cross-species transmission in shared habitats.
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PMID:Distribution of baboon endogenous virus among species of African monkeys suggests multiple ancient cross-species transmissions in shared habitats. 749

We have previously demonstrated the presence of a reverse transcriptase-like enzyme in retroviral particles from patients with essential thrombocythemia, polycythemia vera, and chronic myelogenous leukemia. It was subsequently shown that the human genome contains 50 copies of HERV-K. HERV-K is a human endogenous class I retroviral element that contains gag, pol, and env open reading frames. Using both reverse transcriptase-polymerase chain reaction and ribonuclease protection assays, it is demonstrated that the HERV-K pol is expressed in human blood leukocytes. The data indicates that this expression is restricted in CML white cells and is the result of gene regulation.
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PMID:Expression of human endogenous retrovirus (HERV-K) in chronic myeloid leukemia. 750 41


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