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:2.7.7.48 (transcriptase)
9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two sheep choroid plexus cell cultures were maintained and propagated for 413 days since being infected with strain K796 visna virus. The majority of the cells in these cultures contained visna virus-specific antigen on days 93 and 105 after infection. Reverse transcriptase-like activity similar to that present in visna virus preparations was obtained from these cultures when very little plaque-forming virus was being synthesized. The persistently infected cultures are resistant to the cytopathic effect which occurs in uninfected cultures upon exposure to visna virus. Persistently infected cells require more time than uninfected cells to become confluent. Less than 0.02 percent of the persistently infected sheep choroid plexus cells form macroscopic colonies within 14 days, whereas 20 to 30 percent of the cells from uninfected cultures form macroscopic colonies within this time.
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PMID:Long-term Visna virus infection of sheep choroid plexus cells: initiation and preliminary characterization of the carrier cultures. 4 11

The anti-influenza virus activity of polysaccharides and other high molecular weight fractions from pine cone extract (PCE) of Pinus parviflora Sieb. et Zucc. was investigated. None of the fractions affected the growth of MDCK cells. The acidic PCE substances markedly suppressed the growth of the influenza virus in MDCK cells. Significant inhibition of both the viral protein synthesis in infected cells and virion-associated RNA-dependent RNA polymerase activity was observed with these acidic fractions. Although amantadine inhibited virus plaque formation as effectively as PCE fractions, it was less effective in inhibiting the RNA polymerase activity. These results suggest that PCE, which has been shown to contain antitumor substance(s), also contains anti-influenza virus substance(s).
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PMID:Inhibition of influenza virus infection by pine cone antitumor substances. 233 67

The infectious particles of plaque-derived, low multiplicity passaged wild-type VSV of New Jersey origin consistently induce about 1800 units of interferon (IFN)/10(7) aged chick embryo cells. This inducing capacity is sensitive to both uv radiation and heat (50 degrees). Virus obtained after two successive high multiplicity passages in GMK-Vero cells consistently induced over 25,000 units of IFN/10(7) cells. The IFN induction dose-response curve showed that one IFN-inducing particle (IFP) per cell sufficed to produce a quantum yield of IFN, but infection with two or more IFPs led initially to a marked suppression in the yield of IFN. IFN induction was attributed to two distinct defective particles that differed in size, both containing snap-back RNA, i.e., covalently linked, self-complementary [+/-]RNA. The IFN-inducing capacity of these defective-interfering particles was not inactivated by uv or heat. However heat did eliminate the IFN suppressing activity observed at higher multiplicities, implicating a heat-sensitive component in the virion as a regulator of IFN yield, and involving possibly the virion transcriptase and 3'-leader RNA product.
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PMID:Interferon induction by viruses. XIX. Vesicular stomatitis virus--New Jersey: high multiplicity passages generate interferon-inducing, defective-interfering particles. 247 95

The complete RNA sequence of the L protein gene of lymphocytic choriomeningitis virus (LCMV) is presented. It is the first L protein sequence to be obtained for the Arenaviridae, a family of single-stranded RNA viruses which includes Lassa fever virus, and the Tacaribe complex viruses such as Pichinde and the Argentine and Bolivian hemorrhagic fever viruses. It is the largest open reading frame on the L RNA spanning 6633 nucleotides and coding for a 2210 amino acid protein with a calculated molecular weight of 254,529. Antipeptide sera identify a gene product encoded on the L RNA: it has a mass of approximately 200,000 Da and is found in virions and ribonucleoprotein complexes from infected cells (M. Singh, F. Fuller-Pace, M. J. Buchmeier, and P. J. Southern, 1987, Virology, 161, 448-456). Mutations mapped to the L gene affect plaque morphology (Kirk et al., 1980), the lethality of a virulent LCMV strain on guinea pigs (Y. Riviere, R. Ahmed, P. J. Southern, M. J. Buchmeier, and M. B. A. Oldstone, 1985, J. Virol., 55, 704-709), and the ability of a variant strain of LCMV to suppress the cytotoxic T-cell response and initiate persistent infection (M. Salvato, E. Shimomaye, P. Southern, and M. B. A. Oldstone, 1988, Virology, 164, 517-522; Ahmed et al., 1988). All of these phenotypes indicate that the viral genes on the L strand are critical elements controlling virus replication and the pattern of LCMV infection. The L gene sequence encodes a viral polymerase although this protein bears little resemblance to the published sequences of other RNA virus polymerases. Therefore the LCMV polymerase likely represents a distinct category of viral transcriptase.
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PMID:The primary structure of the lymphocytic choriomeningitis virus L gene encodes a putative RNA polymerase. 270 3

Replication of the infectious RNA genome of poliovirus is accomplished in cells by the viral RNA polymerase through negative-strand RNA intermediates. Full-length negative-strand poliovirus RNA was synthesized in vitro by transcription of infectious poliovirus cDNA with bacteriophage SP6 DNA-dependent RNA polymerase. When provided with this negative-strand RNA as template, the poliovirus RNA-dependent RNA polymerase synthesized full-length positive-strand molecules. The positive-strand RNAs synthesized in vitro were infectious when transfected into HeLa cells. In contrast, positive-strand copies of poliovirus RNA synthesized in vitro by SP6 polymerase, using a poliovirus cDNA template, were not infectious. Production of infectious positive-strand RNA by the poliovirus polymerase was not observed when magnesium or negative-strand RNA template was omitted from the reaction mixture. Infectivity of the product RNA was not destroyed by DNase treatment. The specific infectivity in HeLa cells of in vitro-synthesized positive-strand RNA was 4 X 10(4) plaque-forming units/micrograms of RNA.
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PMID:In vitro synthesis of infectious poliovirus RNA. 300 3

The synthesis of viral RNA by wild-type vesicular stomatitis virus (L(1)VSV) and a small, plaque-size mutant (S(2)VSV) was studied in vitro and in chicken embryo (CE) and mouse L-cell cultures. Virus-specific RNA synthesized in CE or L cells infected with either L(1) or S(2)VSV at low multiplicity was of the same size classes, 12 to 15S, 28S, and 38S. The major differences were in the proportion of RNA produced of each size class. L(1)VSV always synthesized larger proportions of 38S RNA, and S(2)VSV produced larger proportions of 12 to 15S RNA. Both S(2) and L(1)VSV exhibited RNA transcriptase activity in vitro and in cell culture. The products of the in vitro reaction were the same, 12 to 15S for both. The products of the virion-associated transcriptase in CE or L-cell cultures in the presence of cycloheximide were also the same for both viruses but differed from the in vitro products in that 28S and 12 to 15S RNA were made. The effects of addition of cycloheximide at various times after infection demonstrated that new protein synthesis is required early (0-2 h) for both S(2) and L(1)VSV to initiate and maintain the normal rate of viral RNA synthesis. However, the overall rate of RNA synthesis in L(1)VSV infections became independent of protein synthesis after 2 h whereas the rate in S(2)VSV infections did not. With either virus, synthesis of 38S RNA did not occur in the absence of protein synthesis. Moreover, continuous 38S RNA production required continuous protein synthesis. Production of 38S RNA ceased within 30 min after addition of cycloheximide to S(2) (-) or L(1)VSV-infected CE or L cells that had already begun to synthesize the 38S form. The cycloheximide-induced cessation of 38S RNA synthesis was accompanied by a marked increase in production of 12 to 15S and 28S RNA in L(1)VSV-infected cells, but no increase in synthesis of small RNA species occurred in S(2)VSV-infected cells.
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PMID:RNA synthesis by vesicular stomatitis virus and a small plaque mutant: effects of cycloheximide. 435 30

Pyridoxal 5'-phosphate (PLP), a reversible inhibitor of in vitro transcription by fowl plaque virus, has been used to identify the transcriptase. Kinetic analyses showed that PLP competitively inhibits the addition of each nucleoside triphosphate in ApG-primed reactions, suggesting that both initiation and elongation are affected. The irreversible inhibition by PLP following reduction with borohydride was prevented by preincubation with the first substrate: GTP in unprimed reactions or CTP in the presence of ApG. On reaction of FPV proteins with PLP and [3H]borohydride the core protein PB1 was preferentially labeled and the labeling was selectively blocked by GTP or ApG + CTP. These data suggest that PB1 has the nucleotide-binding site of the transcriptase, is responsible for both initiation and elongation, and is apparently associated with the 3' ends of template RNAs in virions.
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PMID:Identification of the influenza virus transcriptase by affinity-labeling with pyridoxal 5'-phosphate. 619 1

A rapid method for production of influenza A virus variants resistant to the adamantane series derivatives, amantadine and remantadine, has been developed. The method consisted of two stages. In the first, the virus was subjected to one passage in the presence of the preparations under a liquid overlayer in a one-cycle experiment. In the second stage, the resulting virus was titrated by the plaque method, the agar overlay containing the preparations in a concentration which was not toxic for the cells. Production of large and small plaques in the presence of the preparations in agar was an indication for selection of resistant virus variants and their further study. Cross-resistance of amantadine- and remantadine-resistant variants to remantadine and amantadine, respectively, was studied. No complete cross-resistance in these viruses could be demonstrated. The amantadine-resistant virus was not inhibited by remantadine, whereas the remantadine-resistant virus was significantly inhibited by amantadine as was demonstrated by both virological methods and by induction of RNA-dependent RNA polymerase and synthesis of viral proteins. The experimental results suggest that the mechanisms of formation of influenza A virus resistance to amantadine and remantadine are not absolutely identical.
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PMID:[Rapid method of producing influenza A virus variants resistant to amantadine and remantadine and their primary characteristics]. 713 21

To generate a collection of conditionally defective poliovirus mutants, clustered charged-to-alanine mutagenesis of the RNA-dependent RNA polymerase 3D was performed. Clusters of charged residues in the polymerase coding region were replaced with alanines by deoxyoligonucleotide-directed mutagenesis of a full-length poliovirus cDNA clone. Following transfection of 27 mutagenized cDNA clones, 10 (37%) gave rise to viruses with temperature-sensitive (ts) phenotypes. Three of the ts mutants displayed severe ts plaque reduction phenotypes, producing at least 10(3)-fold fewer plaques at 39.5 degrees C than at 32.5 degrees C; the other seven mutants displayed ts small-plaque phenotypes. Constant-temperature, single-cycle infections showed defects in virus yield or RNA accumulation at the nonpermissive temperature for eight stable ts mutants. In temperature shift experiments, seven of the ts mutants showed reduced accumulation of viral RNA at the nonpermissive temperature and showed no other ts defects. The mutations responsible for the phenotypes of most of these ts mutants lie in the N-terminal third of the 3D coding region, where no well-characterized mutations responsible for viable mutants had been previously identified. Clustered charged-to-alanine mutagenesis (S. H. Bass, M. G. Mulkerrin, and J. A. Wells, Proc. Natl. Acad. Sci. USA 88:4498-4502, 1991; W. F. Bennett, N. F. Paoni, B. A. Keyt, D. Botstein, J. J. S. Jones, L. Presta, F. M. Wurm, and M. J. Zoller, J. Biol. Chem. 266:5191-5201, 1991; and K. F. Wertman, D. G. Drubin, and D. Botstein, Genetics 132:337-350, 1992) is designed to target residues on the surfaces of folded proteins; thus, extragenic suppression analysis of such mutant viruses may be very useful in identifying components of the viral replication complex.
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PMID:Clustered charged-to-alanine mutagenesis of poliovirus RNA-dependent RNA polymerase yields multiple temperature-sensitive mutants defective in RNA synthesis. 828 89

A previous report described the recovery from cDNA of infectious recombinant respiratory syncytial virus (RSV) strain A2 (P. L. Collins, M. G. Hill, E. Camargo, H. Grosfeld, R. M. Chanock, and B. R. Murphy, Proc. Natl. Acad. Sci. USA, 92:11563-11567, 1995). Here, the system was used to construct recombinant RSV containing an additional gene encoding chloramphenicol acetyltransferase (CAT). The CAT coding sequence was flanked by RSV-specific gene-start and gene-end motifs, the transcription signals for the viral RNA-dependent RNA polymerase. The RSV-CAT chimeric transcription cassette was inserted into the region between the G and F genes of the complete cDNA-encoded positive-sense RSV antigenome, and infectious CAT-expressing recombinant RSV was recovered. Transcription of the inserted gene into the predicted subgenomic polyadenylated mRNA was demonstrated by Northern (RNA) blot hybridization analysis, and the encoded protein was detected by enzyme assay and by radioimmunoprecipitation. Quantitation of intracellular CAT, SH, G, and F mRNAs showed that the CAT mRNA was efficiently expressed and that the levels of the G and F mRNAs (which represent the genes on either side of the inserted CAT gene) were comparable to those expressed by a wild-type recombinant RSV. Consistent with this finding, the CAT-containing and wild-type viruses were very similar with regard to the levels of synthesis of the major viral proteins. Each of 25 RSV isolates obtained by plaque purification following eight serial passages expressed CAT, showing that the foreign gene was faithfully maintained in functional form. Analysis by reverse transcription and PCR did not reveal evidence of deletion of the foreign sequence. This finding demonstrated that the RSV genome can accept and maintain an increase in length of 762 nucleotides of foreign sequence and can be engineered to encode an additional, 11th mRNA. The presence of the additional gene resulted in a 10% decrease in plaque diameter and was associated with delay in virus growth and 20-fold decrease in virus yield in vitro. Thus, introduction of an additional gene into the RSV genome might represent a method of attenuation. The ability to express foreign genes by recombinant RSV has implications for basic studies as well as for the development of live recombinant vaccines.
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PMID:Recovery of infectious respiratory syncytial virus expressing an additional, foreign gene. 879 98


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