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)

The presence of an RNA-dependent RNA polymerase is demonstrated in purified rotavirus particles. Optimum polymerase activity was found between 45 to 50 degrees C, at pH 8, and in the presence of 10 mM-magnesium ions. The polymerase product was highly sensitive to pancreatic RNase (97%) in low or high salt concentration. The enzyme was activated by EDTA treatment of intact particles or heat shock. The similarities between reovirus, blue-tongue virus and rotavirus polymerases are discussed.
J Gen Virol 1977 Sep
PMID:Ribonucleic acid polymerase activity associated with purified calf rotavirus. 2 Dec 25

Reverse transcriptase activity was detected in the supernatants of rat embryo fibroblast cell cultures transformed by HSV types 1 and 2 at either the sub-optimal temperature of 20 degrees C or the supra-optimal temperature of 42 degrees C. Rat cells clones which had been transformed at 20 degrees C contained higher levels of C-type virus DNA polymerase than did cell clones which had been transformed at 42 degrees C. Syncytia formation typical for C-type RNA viruses occurred at passages higher than 24. The activation of endogenous C-type RNA viruses was independent of the virus and transformation method used.
J Gen Virol 1977 Aug
PMID:Activation of an endogenous C-type RNA virus in rat embryo cells after transformation by herpes simplex virus types 1 and 2. 7 May 8

LLC-MK2 cells chronically infected with two strains of rubella virus, HPV-77 and Thomas, have been examined over several months to find out the mechanism of persistence. Evidence is given for the presence of defective particles in these cultures by finding virion RNA which sedimented at 12S instead of the 40S typical of the fully infectious virus. A 'provirus' DNA copy of the rubella virus genome was not detected by methods which included filter hybridization and in situ hybridization, or by treatment of the chronically infected cells with mitomycin C, antinomycin D or 5-bromodeoxyuridine. In addition, the chronically infected cells contained RNA-dependent RNA polymerase activity, but no RNA-dependent DNA polymerase activity.
J Gen Virol 1979 May
PMID:Mechanism of persistence of rubella virus in LLC-MK2 cells. 11 97

Human cells derived from both normal and neoplastic tissues can be infected by Mason-Pfizer monkey virus (MPMV) without accompanying cytopathology. Infection of cell cultures such as human rhabdomyosarcoma (A204) results in a persistenly infected cell line which can be subcultured over 30 sequential culture passages without significant change in phenotype properties according to reverse, transcriptase (RT), MPMV p27 antigen content, virus particle count and infectivity titre. Productive virus infections were established at relatively low virus particle (VP) input multiplicities (p.i.m.; about 0.06 VP/cell) In A204 cell cultures. At higher p.i.m. (about 600 to 6000 VP/cell) newly synthesized virus was detected within 4 days post infection. Although virus production was cumulative following primary infection, after subculture of infected cultures MPVM production was greater during active cell division. Using synchronization techniques, MPMV replication in persistently infected cultures was found to be cell cycle-dependent. The major internal antigen, p27, was synthesized in G2 and newly synthesized virus particles were released predominantly during mitosis and early G1. Colcemid arrest of cells during mitosis inhibited subsequent MPMV release. Consequently, production of extracellular virus depends upon the progression of cells through the mitotic stage. These data, which provided a basic understanding of the virus-host relationship that occurs in primate cells productively infected with MPMV, were used as a guideline for isolating MPMV-like viruses from experimentally and naturally infected Rhesus monkey.
J Gen Virol 1979 Aug
PMID:Characterization of infection and replication of Mason-Pfizer monkey virus in human cell cultures. 11 35

The poliovirus replication complex was isolated and purified from infected HeLa S3 cells. Preparations with RNA-dependent RNA polymerase activity were concentrated 200- and 1000-fold with respect to the original virus and total protein content. The enzyme activity was found to be associated with the proteins NCVPI, 2, 3, 4, (5), 6 and VPl/NCVPx. The structural proteins VP2, 3 and 4 were not present. Addition of cycloheximide to infected cells resulted in a decrease in the in vitro polymerase activity and a loss in NCVPI content. Treatment of the infected cells with toloylsulphonyl-phenylalanine chloromethyl ketone (TPCK) and iodoacetamide (IAA) led to an inhibition of in vivo RNA synthesis. The 750 g supernatant fluids obtained from extracts of these cells were able to block RNA synthesis in vitro. Electrophoretic profiles of the respective protein compositions indicate that large virus precursor proteins are responsible for the inhibition of poliovirus RNA synthesis in vivo and in vitro.
J Gen Virol 1975 Jul
PMID:Virus-specific proteins associated with the replication complex of poliovirus RNA. 16 19

Two newly synthesized pyrimidine derivatives were found to possess antiviral activity against Mengovirus in Fogh and Lund (FL) cells and in a cell-free system. The inhibitory effect on RNA-dependent RNA polymerase of Mengovirus-infected FL cells was assayed using 14C-UTP as precursor. Addition of 50 or 100 muM of the inhibitors in a cell-free system of crude enzyme and nucleoside triphosphate medium for 60 min incubation at 37 degrees C resulted in about 40 to 60% lower counting rates for drug-treated reaction mixtures. The analysis of the polymerase synthesis product (virus RNA extracted from the cell-free reaction mixture and deproteinized by the phenol-SDS method) was carried out by means of agarose-acrylamide gel electrophoresis. The main finding was a reduction of single-stranded Mengovirus RNA (RNase-sensitive and LiCl-precipitable). The rates of synthesis of the replicative intermediate (LiCl-precipitable) and the replicative form of RNA (LiCl-soluble) were not significantly influenced.
J Gen Virol 1977 Jan
PMID:Effects of pyrimidine derivatives on RNA-dependent RNA polymerase of mengovirus-infected Fogh and Lund (FL) cells. 18 80

In cultures of Ly cells treated with 10 or 30 reference units/ml of mouse interferon there was a 30 to 200 times reduction in the production of infectious vesicular stomatitis virus (VSV); virus particle production, as measured by VSV particle associated virus RNA, virus protein, and virus transcriptase, was inhibited by, at most, six times. These results suggested that interferon-treated cells produce VSV particles with low infectivity and resemble the findings in interferon-treated cells infected with murine leukaemia viruses.
J Gen Virol 1979 Jul
PMID:Production of vesicular stomatitis virus with low infectivity by interferon-treated cells. 22 98

The RNA-dependent RNA polymerase induced in BHK 21 cells by infection with foot-and-mouth disease virus has been isolated from the replication complex. It contains a major, virus-coded protein with mol. wt. 56 000 which appears from serological studies and tryptic peptide mapping to be the same as the virus infection associated (VIA) antigen and the protein P56 found in cells infected with the virus. Other virus coded proteins and a host cell protein were present in the partially purified replication complex but were removed by digestion with ribonuclease T1, leaving only the major virus coded protein. The tryptic peptide maps of the VIA antigen of the seven serotypes of the virus were similar, suggesting a high level of conservation in that region of the genome coding for the RNA polymerase of each type.
J Gen Virol 1979 Nov
PMID:Purification and identification of the RNA-dependent RNA polymerase of foot-and-mouth disease virus. 23 34

Recombinants of human influenza type A viruses, A/Krasnodar/101/1959 (H2N2) or A/Habarovsk/15/1976 (H3N2), and fowl plague virus (FPV), strain Weybridge (Hav1Neq1) were obtained. The genome of the recombinant obtained by recombination of influenza A/Habarovsk/15/1976 virus and FPV contained the genes 4 (HA) and 6 (NA) derived from the influenza A/Habarovsk virus and all the other genes [1, 2, 3, 5 (NP), 7 (M), 8 (NS)] from FPV. The genome of the recombinant of A/Krasnodar/101/1959 virus and FPV contained the genes 2, 4 (HA) and 6 (NA) derived from influenza A/Krasnodar virus and all the other genes [1, 3, 5, (NP), 7 (M), 8 (NS)] from FPV. The recombinants, like FPV, gave high virus yields in chick embryos and could multiply at high temperatures (40 and 42 degrees C), but, like human influenza viruses, were non-pathogenic for chickens and did not replicate in chick embryo fibroblast culture, but did replicate in a human conjunctiva cell line, clone 1-5C-4. The virion transcriptase of the recombinants, in a number of properties determined in vitro, was similar to FPV transcriptase but not to the human influenza virus enzyme.
J Gen Virol 1979 Apr
PMID:Investigation of recombinants of human influenza and fowl plague viruses. 47 41

RNA 1 (see end of Summary) of a cold-adapted and temperature-sensitive (ts) influenza virus mutant A/Ann Arbor/6/60 has a different mobility from RNA 1 of wild-type (wt) A/Ann Arbor/6/60 when subjected to electrophoresis through acrylamide/agarose gels in the absence of denaturing agents. Detection of this lesion in RNA 1 of the mutant virus was dependent on the temperature of the gel during electrophoresis. Because RNA 1 is believed to code for a protein involved in virus-specific RNA synthesis we compared phenotypes of virion transcriptases in the wt and mutant viruses. The enzyme of the mutant virus was found to be about 40% less active at 40 degrees C than the enzyme of the wt virus when related to their activities at 31 degrees C. Two cold-adapted ts recombinants which derive their RNA 1 from the mutant A/Ann Arbor/6/60 have virion transcriptases with a phenotype similar to that of their mutant parent. Three different cold-adapted ts recombinants, however, which also derive their RNA 1 from the mutant A/Ann Arbor/6/60, have virion transcriptases with a phenotype similar to that of wt virus. We conclude, therefore, that the conditional-lethal ts property of A/Ann Arbor/6/60 mutant and its recombinants is independent of the phenotypic marker observed for the A/Ann Arbor/6/60 mutant virion transcriptase, and that the lesion in RNA 1 of the mutant may also be unrelated to the observed difference between virion transcriptases of the mutant and wt A/Ann Arbor/6/60 viruses. The phenotypes of the virion transcriptases in recombinants did, however, correlate with the derivation of their RNA 2. This suggests that the increased temperature-sensitivity of virion transcriptase of the A/Ann Arbor/6/60 mutant is caused by either (1) a lesion (not necessarily conditionally lethal) that occurred in its RNA 2 during the course of cold-adaptation, or (2) a lesion in another gene whose product is a component of the virion transcriptase complex, but which lesion is only expressed phenotypically when there is a synergistic interaction in the transcriptase complex with the product of A/Ann Arbor/6/60 rna 2.
J Gen Virol 1979 Aug
PMID:Comparative studies of wild-type and cold-mutant (temperature-sensitive) influenza viruses: independent segregation of temperature-sensitivity of virus replication from temperature-sensitivity of virion transcriptase activity during recombination of mutant A/Ann Arbor/6/60 with wild-type H3N2 strains. 52 98


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