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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)

Adsorption of murine leukaemia virus (MLV) to NIH/3T3 cells, as determined by analysing its reverse transcriptase activity in the cell membrane, was found to be unaffected by interferon (IFN). Virus penetration and uncoating were followed by quantifying intracellular virions in terms of sedimentable reverse transcriptase activity in the cytoplasmic fraction. The penetrating virions were found to accumulate to a higher level in IFN-treated cells than in untreated controls. Intracellular virions were uncoated in untreated cells shortly after their penetration, whereas their uncoating was delayed in the IFN-treated cells for 2 to 3 h. Neither virus uncoating nor the effect of IFN on this process appeared to require new protein synthesis, since both were unaffected by cycloheximide (CH).
J Gen Virol 1980 Dec
PMID:An effect of interferon on the uncoating of murine leukaemia virus not related to the antiviral state. 616 46

The effect of human fibroblast interferon (IFN), a heterologous IFN, on the uncoating of murine leukaemia virus (MLV) was investigated in exogenously infected NIH/3T3 mouse cells. Virus uncoating was determined by following the disappearance of the penetrating virus particles from the cytoplasm of the infected cells. Intracellular virus particles were estimated by sedimenting them at high speed from the cytoplasmic fraction of the infected cells and assaying their reverse transcriptase activity. In untreated control cells, uncoating started immediately after penetration, but in cells treated with human IFN, uncoating was delayed for 2 to 3 h. This delay led to prolongation of the infectious cycle, with delayed release of progeny virus. The delay in release did not result from inhibition by IFN of the process of release, since in NIH/3T3 cells chronically infected with MLV, treatment with IFN had no effect on virus release.
J Gen Virol 1980 Dec
PMID:Effect of human fibroblast interferon on uncoating and release of murine leukaemia virus in NIH/3T3 mouse cells. 616 47

Polyinosinic acids containing methyl and sulphur substitutions are potent inhibitors of reverse transcriptase. Substitution of sulphur for oxygen at the 6 position produces significant effects on the properties of polyinosinic acid: the kinetics of inhibition change from competitive to mixed-type and the inhibition constant falls by three orders of magnitude. In contrast, 1-methyl substitution produces no such effects. Poly(1-methyl-6-thioinosinic acid) or poly(m1s6I) inhibits irreversibly, inhibiting all ten reverse transcriptases tested under a variety of assay conditions. In cell culture test systems, poly(m1s6I) is capable of blocking both infection by non-transforming viruses and transformation by a sarcoma virus. The presence of poly(m1s6I) in a preinfected culture results in the production of non-infectious virus particles lacking reverse transcriptase activity.
J Gen Virol 1981 Feb
PMID:Antiviral properties of polyinosinic acids containing thio and methyl substitutions. 616 84

We have studied the virus-like 30S (VL30) RNA sequences of mice. Previous work has shown that these sequences are coded in the mouse genome, expressed in some normal cells and released as pseudotypic particles from cells producing murine C-type retroviruses. VL30 sequences have some similarities to standard retrovirus RNA, but differences also exist. To further assess the similarities and differences, several aspects of VL30-specific metabolism were investigated. We studied the initiation of VL30-specific DNA synthesis during an endogenous reverse transcriptase reaction. Short initial VL30-specific cDNA transcripts were covalently attached to RNA as measured by equilibrium banding in caesium sulphate density gradients. Therefore, reverse transcription of VL30-specific cDNA is initiated by an RNA primer. The intracellular synthesis of VL30 RNA was investigated by pulse labelling uninfected JLS-V9 cells with 3H-uridine. Hybridization of the pulse-labelled nuclear RNA indicated that the major VL30-specific RNA evident after a 15 min label was the same size as the mature VL30 RNA. Thus, VL30 RNA is apparently not synthesized via a higher mol. wt. precursor. Both of these results demonstrate similarity of VL30 RNA sequences to standard retroviruses. One unique feature of VL30 RNA was detected. JLS-V9 cells contained both the monomeric VL30 RNA and a hydrogen-bonded 38S form which yielded the monomer when denatured. This contrasts with standard murine leukaemia virus which is only found as a monomer within cells.
J Gen Virol 1981 Jun
PMID:Further characterization of virus-like 30S (VL30) RNA of mice: initiation of reverse transcription and intracellular synthesis. 616 92

The avian RNA tumour virus structural protein p12 was purified from avian myeloblastosis virus (AMV) by nucleic acid affinity chromatography to apparent homogeneity as judged from SDS--polyacrylamide gel electrophoresis. A filter binding assay was used for the identification of p12. High concentrations of p12 precipitated nucleic acids out of solution in the absence of MgCl2. Binding of p12 to single-stranded nucleic acids protected them from digestion with nucleases and resulted in a hyperchromic effect. These phenomena were reversible in the presence of salt. The affinity of p12 to nucleic acids was determined by competing for the binding of p12 to denatured radioactive DNA by various other nuclei acids. It was found that p12 bound preferentially to single-stranded nucleic acids and showed a higher affinity to poly(rI) than to poly(rC) and poly(rA). Purified RNA-dependent DNA polymerase activity from AMV was stimulated up to sixfold by p12, depending on the template. Solubilization of RNA in RNA--DNA hybrids by RNase H was inhibited in the presence of p12.
J Gen Virol 1981 Aug
PMID:Properties of the avian viral protein p12. 616 96

An ecotropic type C retrovirus (D1-MuLV) isolated from SJL/J mice was injected into neonatally thymectomized SJL/J mice. There was no acceleration of development of reticulum cell neoplasm (RCN) in these mice as compared with the control, uninoculated but similarly thymectomized group. The incidence of RCN at 10 and 11 months after injection was 14.6% and 12.5% respectively. Two female mice inoculated with D1-MuLV developed mammary adenocarcinoma. There was persistence of high titres of the ecotropic virus associated with RCN and mammary tumour of SJL/J mice. Xenotropic virus (X-MuLV) was detected in spleens of normal SJL/J mice at ages 6 and 12 months (60% and 80% respectively) but not at other ages. The X-MuLV isolated from SJL/J mouse embryo cell cultures treated with 5-iodo-2'-deoxyuridine (SJL-MEF-X-MuLV) and that isolated from a spontaneous RCN (SJL-RCN-X-MuLV) were compared with NZB-X-MuLV (NZB mouse origin) and AT124-X-MuLV (NIH Swiss mouse origin) in regard to their host range, ion and primer-template preference by reverse transcriptase, virus interference and neutralization characteristics. Cross-neutralization and gp70 competitive radio-immunoassays showed that D1-MuLV is more closely related to AKR-MuLV than to Rauscher-MuLV and appears to share some virus envelope antigens with SJL-X-MuLVs. The type-specific gag gene product (p12) from Balb:virus-2 and NZB-X-MuLV was used in competitive radioimmunoassay, and SJL-RCN-X-MuLV was found to be more closely related to Balb:virus-2 (MuLV-X alpha) than to NZB-X-MuLV (MuLV-X beta).
J Gen Virol 1981 Nov
PMID:Ecotropic and xenotropic type C retroviruses associated with reticulum cell neoplasms of SJL/J mice. 617 51

Model systems to study restricted primate retrovirus expression were established by de novo infection of canine foetal thymus cells (CF-2Th) and superinfection of HEL-12 cells with HEL-12 virus. In the resulting CF-2Th/HEL-12V cells and HEL-12/HEL-12V cells, four sequential stages of virus infection were defined by the production of reverse transcriptase (RT)-containing particles and expression of virus antigens as detected by radioimmunoassays. Stage 1 cells did not synthesize virus antigens or produce RT-containing particles. Stage 2 cells synthesized virus antigen but not RT-containing particles. Stage 3 cells synthesized antigen and produced RT-containing particles, and stage 4 cells synthesized virus antigens but no longer produced RT-containing particles. The duration of the four stage infection is 2 to 3 weeks in both cell types. Monospecific competition radioimmunoassays to detect HEL-12V p30 or gp70 antigen showed high levels of virus antigen throughout stages 2 to 4 of infection. Analysis of immunoprecipitates formed under conditions to detect either p30- or or gp70-containing proteins in cells pulsed and pulsed--chased with [3H]leucine showed the same spectrum of virus precursor polyproteins, intermediates and mature virion components in stage 2 to 4 cells in canine and human infections. Spent culture fluids collected from stage 3 and stage 4 CF-2Th/HEL-12V cells failed to reveal inhibitors of RT activity. Stage 4 CF-2Th/HEL-12V or HEL-12/HEL-12V cells labelled with [3H]uridine produced virions which incorporated [3H]uridine but did not have RT activity, suggesting that restricted infection is characterized by production of HEL-12V defective in RT activity.
J Gen Virol 1981 Dec
PMID:Restricted HEL-12 virus infections in de novo infected human and canine cells. 617 57

The effects of microtubule-depolymerizing agents on virion production in MJD-54 cells chronically infected with Moloney murine leukaemia virus were examined. By measuring the amount of reverse transcriptase activity remaining in particles recovered from culture fluids, we found that incubation with 1 microM- or 10 microM-colchicine, vinblastine or nocodazole resulted in 30 to 40% decreases in virus production. The decrease in virus production did not seem to be due to general damage to the cells since cellular RNA and protein synthesis were only slightly, if at all, inhibited by the drug treatment (less than 10%). Furthermore, virus proteins accumulated inside drug-treated cells, viz, [35S]methionine-labelled Pr65gag showed a 1.5-fold increase over a 3 h continuous label interval. Consistent with this accumulation of virus protein, electron microscope studies showed that inside drug-treated cells ther was a 2- to 2.5-fold accumulation of virions within cytoplasmic vesicles. All of these results support the idea that cytoplasmic microtubules play a role in the production of murine leukaemia virus.
J Gen Virol 1982 Feb
PMID:Microtubule-depolymerizing agents inhibit Moloney murine leukaemia virus production. 617 83

The effects of interferon treatment on the expression of murine mammary tumour virus (MuMTV) by a continuous mammary tumour cell line of GR mouse were investigated. Interferon markedly inhibited the excretion of MuMTV particles in the culture media as measured by hybridization of virus-specific RNA and virus-associated reverse transcriptase activity. There was no inhibition of virus RNA and protein synthesis in those conditions. The steady-state level of intracellular virus RNA and its rate of synthesis were not modified by interferon treatment. The intracellular levels of the major virus envelope and core proteins as measured by immunoprecipitation techniques remained unchanged. Interferon failed to inhibit the synthesis and the processing of the gp52 glycoprotein and p27 core protein precursors. However, the rate of maturation of the glycoprotein precursor was slowed down. Surface labelling of intact cells did not reveal accumulation of virus proteins on the cell membrane upon interferon treatment. The intracellular level of MuMTV-characteristic reverse transcriptase activity was reduced in interferon treated cells, although to a lower extent than extracellular virion-associated enzyme activity. MuMTV particles released from interferon-treated cells revealed no difference in their protein composition. These results are consistent with an inhibition by interferon of a late step in the replication of MuMTV.
J Gen Virol 1982 Sep
PMID:Effects of interferon on the expression of mouse mammary tumour virus in GR cells. 618 67

We have previously reported that among a series of human tumours investigated, only human teratocarcinoma cell lines derived from testicular tumours or pulmonary metastases of patients in Germany and the U.S.A. produced retrovirus-like particles spontaneously, albeit in low amounts. In a recent publication electron microscopical data suggested that the human teratocarcinoma-derived ( HTD ) particles were morphologically closely related, but not identical, to the type C retroviruses of animals. In this communication, the explantation of three human teratocarcinoma cell lines is briefly described. Evidence is presented that HTD particles (i) are synthesized only in a fraction of the epithelioid and differentiating cells; (ii) can be induced biochemically in a manner characteristic of retroviruses; (iii) either are not infectious or possess a peculiar host range; (iv) are immunologically unrelated to animal retrovirus strains; (v) possess an endogenous RNA-dependent DNA polymerase activity that can be banded at 1.16 g/ml in linear sucrose gradients. These results may be taken as suggestive evidence that HTD particles represent a novel group of unique retroviruses.
J Gen Virol 1984 May
PMID:Human teratocarcinomas cultured in vitro produce unique retrovirus-like viruses. 620 29


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