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:2.7.7.6 (RNA polymerase)
34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Defective interfering (DI) particles of equine herpesvirus type 1 (EHV-1) are capable of mediating persistent infection (S. A. Dauenhauer, R. A. Robinson, and D. J. O'Callaghan, J. Gen. Virol. 60:1-14, 1982; R. A. Robinson, R. B. Vance, and D. J. O'Callaghan, J. Virol. 36:204-219, 1980). Sequence analysis of cloned DI particle DNA revealed that portions of two regulatory genes, ICP22 (IR4) and ICP27 (UL3), are linked in frame to form a unique hybrid open reading frame (ORF). This hybrid ORF, designated as the IR4/UL3 gene, encodes the amino-terminal 196 amino acids of the IR4 protein (ICP22 homolog) and the carboxy-terminal 68 amino acids of the UL3 protein (ICP27 homolog). Portions of DNA sequences encoding these two regulatory proteins, separated by more than 115 kbp in the standard virus genome, were linked presumably by a homologous recombination event between two identical 8-bp sequences. Reverse transcriptase-PCR and S1 nuclease analyses revealed that this unique ORF is transcribed by utilizing the transcription initiation site of ICP22 and the polyadenylation signal of ICP27 in DI particle-enriched infection. Immunoprecipitation and Western blot (immunoblot) analyses with antisera to the ICP22 and ICP27 proteins demonstrated that a 31-kDa hybrid protein was synthesized in the DI particle-enriched infection but not in standard virus infection. This 31-kDa hybrid protein was expressed at the same time as the ICP22 protein in DI particle-enriched infection and migrated at the same location on polyacrylamide gel electrophoresis as the protein expressed from a cloned IR4/UL3 expression vector. These observations suggested that the unique IR4/UL3 hybrid gene is expressed from the DI particle genome and may play a role in DI particle-mediated persistent infection.
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PMID:Expression of an equine herpesvirus 1 ICP22/ICP27 hybrid protein encoded by defective interfering particles associated with persistent infection. 852 42

The phenotypic defects of two mutants of vaccinia virus, the lesions of which map to gene G2R, were characterized in vivo, and the results suggest a role for the G2R protein in viral transcription elongation. Both a temperature-sensitive mutant, Cts56, and an isatin-beta-thiosemicarbazone-dependent deletion mutant, G2A, in gene G2R have a characteristic and unique defect in late viral gene expression. The G2R mutants synthesize early viral RNA, early viral proteins, and viral DNA normally under nonpermissive conditions. In G2R mutants, late viral protein synthesis begins at the normal time, low-molecular-weight viral proteins are synthesized in normal quantities, but synthesis of high-molecular-weight viral proteins is reduced in amount. Intermediate and late promoter utilization is normal in G2R mutants, but intermediate and late RNAs are reduced in size. The reduction in length of the intermediate and late mRNAs represents a truncation of mRNA 3' ends. Thus, intermediate and late RNAs are too short to encode large proteins but long enough to encode small proteins, therefore accounting for the protein synthesis phenotype. These results suggest that the G2R protein acts to regulate the elongation potential of the viral RNA polymerase late during a vaccinia virus infection.
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PMID:Phenotypic characterization of mutants in vaccinia virus gene G2R, a putative transcription elongation factor. 852 60

Lack of an in vitro culture system for human hepatitis B virus has hampered the ability to address fundamental questions regarding the viral life cycle and the effect of viral gene products during productive infection. To study the activity of HBV X protein (HBx) in the context of a viral infectious cycle, we provided HBx in trans during adenovirus infection of liver-derived cells. In hepatoma cells infected with adenovirus mutants deficient in expression of various E1A products, HBx was able to partially substitute for the transcriptional activation function of E1A. HBx also activated adenovirus replication, but to a lesser extent than the activation of transcription. Adenovirus genes transcribed by either RNA polymerase II or RNA polymerase III were activated by HBx during infection. These results suggest that HBx and E1A activate transcription by a similar mechanism and that this viral infection system will be useful for characterization of the functional activities of HBx.
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PMID:Hepatitis B virus X protein partially substitutes for E1A transcriptional function during adenovirus infection. 860 73

Two-hundred Mexican children monitored from birth to 2 years of age in a cohort study of diarrhea were tested for Norwalk virus (NV) and Norwalk-related virus infection. Blood was collected quarterly and tested by an enzyme immunoassay (EIA) using the recombinant NV (rNV) particles as antigen. Stool was collected weekly and tested by an EIA using hyperimmune anti-sera from animals immunized with rNV and a reverse transcription-polymerase chain reaction (RT-PCR) with primers in the RNA polymerase region of NV. A high prevalence of serum antibody to NV (85% at age 2 years) was found by the antibody EIA. In 54 stool specimens selected from children who developed a high titer of serum antibody to rNV, none was positive for NV by the antigen EIA, but 6 yielded products by the RT-PCR. One stool specimen (MX virus) yielded a 3.3 kb RT-PCR product from the 3' end of the viral genome. The MX virus cDNA has a genomic organization like other caliciviruses. Sequence comparison showed that MX virus shares 80% nucleic acid and 91% amino acid sequence identity with Snow Mountain agent (SMA), but only 62% and 60% identity, respectively, with NV in the RNA polymerase region, suggesting that MX virus is a SMA-like virus.
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PMID:Study of Norwalk-related viruses in Mexican children. 863 96

Both genetic and environmental factors appear to contribute to the causation of schizophrenia. Evidence indicating that fetal development is disrupted in schizophrenia and the finding of an excess of winter births among schizophrenic patients have led to continued speculation that an intrauterine viral infection may cause developmental lesions, genetic mutations, or persistent infections that lead to schizophrenia. Certain unique characteristics of the retroviruses render them plausible as candidate "schizoviruses" and the involvement of an endogenous retrovirus would be compatible with some of the puzzling epidemiological findings in schizophrenia. Reverse transcriptase (RT) is a retrovirally encoded enzyme essential for retroviral integration into host DNA. While attempts to detect retroviral infections by measuring RT activity in the peripheral lymphocytes and serum of schizophrenic patients have been unsuccessful, such negative findings may simply mean that the virus is not active in peripheral lymphocytes. A more sensitive and comprehensive approach to detect a retrovirus is to search the genomes of schizophrenic patients directly for the presence of retroviral DNA sequences encoding RT and one possible approach is described.
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PMID:Retroviruses and schizophrenia revisited. 867 9

Tick-transmitted Thogoto and Dhori viruses share structural and genetic properties with the influenza viruses. Here, we compare different steps of their replication cycle in mammalian cells in comparison with influenza A virus. Viral antigens of both viruses accumulated in the nuclei of infected cells, suggesting a nuclear phase of viral replication. Furthermore, as observed with influenza viruses, transcription of Thogoto and Dhori viruses was inhibited by alpha-amanitin and actinomycin D, suggesting a dependence of viral transcription on cellular RNA polymerase II activity. In contrast to influenza viruses, Thogoto and Dhori virus infection did not lead to down-regulation of cellular protein synthesis indicating marked differences regarding the fate of infected cells.
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PMID:Thogoto and Dhori virus replication is blocked by inhibitors of cellular polymerase II activity but does not cause shutoff of host cell protein synthesis. 885 36

In the present study the effect of the attenuated strain TC-83 of the Venezuelan Equine Encephalitis virus on the nuclear transcription in brain cells of rats was assessed. The transcription activity of the DNA depending RNA polymerases (types I and II) in the isolated nuclei of brain of infected rats and controls was determinated by incorporation of the (3H) UTP. Simultaneously a viral replication curve in the brain and the serum was carried out by plaque forming method in chicken embryo cell cultures. RNA polymerase I activity was only significantly reduced after 25 hours of infection, respect to control values, while polymerase II activity was progressive and significantly diminished from inicial stages of the viral infection at 10, 15, 20 y 25 hours post-infection compared to control values. The virus was not detected in the brain but after 25 hours post-infection with very low titers (< 0.7 log10 P.F.U./ml.), while the viral presence in the blood was demonstrated after a 10 hour period. Our results demonstrated a marked effect of the attenuated strain on the brain nuclear transcription, although the presence of the virus was not detected in the brain of the infected rats. This finding suggest a mechanism of action which deserves further studies to elucidate the cerebral metabolic response and the pathogenesis of the Venezuelan Equine Encephalitis infection.
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PMID:[Effect of the attenuated strain (TC-83) of Venezuelan equine encephalitis virus on nuclear transcription in rat brain cells]. 892 28

Nearly 1 000 000 copies of Alu interspersed elements comprise approximately 5% of human DNA. Alu elements cause gene disruptions by a process known as retrotransposition, in which dimeric Alu RNA is a presumed intermediate. Dimeric Alu transcripts are labile, giving rise to stable left monomeric scAlu RNAs whose levels are tightly regulated. Induction of Alu RNA by viral infection or cell stress leads to a dramatic increase in dimeric Alu transcripts, while scAlu RNA increases modestly. Each monomer of the dimeric Alu element shares sequence homology with the 7SL RNA component of the signal recognition particle (SRP). The SRP protein known as SRP9/14 is also found in a discrete complex with scAlu RNA, although whether dimeric Alu RNA is associated with SRP9/14 had been unknown. Here we show that antiserum to human SRP9 immunoprecipitates both scAlu RNA and dimeric Alu RNAs and that these RNPs accumulate after adenovirus infection, while levels of SRP9, SRP14, SRP54 and 7SL SRP RNA are unaffected. Dimeric Alu RNAs are also associated with the La protein, indicating that these are indeed nascent RNA polymerase III transcripts. This report documents that induced Alu transcripts are assembled into SRP9/14-containing RNPs in vivo while SRP levels are unchanged. Implications for Alu RNA metabolism and evolution are discussed.
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PMID:Monomeric scAlu and nascent dimeric Alu RNAs induced by adenovirus are assembled into SRP9/14-containing RNPs in HeLa cells. 893 67

Bronchial epithelial cells are primary sites of airway viral infection, and these cells may play an important role in the pathogenesis of respiratory diseases. It has recently been reported that bronchial epithelial cells express RANTES. RANTES attracts monocytes, T cells, eosinophils, and basophils; it can also activate eosinophils. To determine whether viral infection induces RANTES expression on bronchial epithelial cells, we infected a bronchial epithelial cell line, NCI-H292, with influenza virus A (H3N2). We then examined the concentration of RANTES in the culture medium of infected cells by ELISA and assessed expression of the gene for RANTES by the reverse-transcriptase polymerase chain reaction. We also investigated the concentrations of IL-6, IL-8, and granulocyte-macrophage colony-stimulating factor in the medium of infected cells, because some virus infections have been reported to induce expression of these cytokines on bronchial epithelial cells, but there are few data concerning influenza virus infection. Small amounts of IL-6 and IL-8 were detected in the medium of uninfected cells. RANTES was not detected in the medium of uninfected cells. After influenza virus infection, significant amounts of IL-6, IL-8, and RANTES were released into the culture medium of infected cells, and RANTES messenger RNA was detected from infected cells. Granulocyte-macrophage colony-stimulating factor was not detected in the medium of uninfected and infected cells. These results suggest that influenza virus infection may stimulate production of IL-6, IL-8, and RANTES from human bronchial epithelial cells and that these cytokines may contribute to the pathogenesis of airway inflammatory diseases caused by influenza virus infection.
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PMID:Expression of IL-6, IL-8, and RANTES on human bronchial epithelial cells, NCI-H292, induced by influenza virus A. 897 9

Dialysable Leucocyte Extract (DLE) is a low molecular weight dialysable material of disrupted peripheral human leucocytes with widespread effects on the immune system. We described the in vitro anti-HIV activity of DLE as well as its three chromatographic fractions (Fa, Fb and Fc). To determine the levels of inhibition on HIV replication by DLE we infected MT-4 cell cultures, using the Bru viral isolate at 0.05, 0.1, 0.5 and 1 m.o.i. Previously, MT-4 cells cultures were treated with DLE or fractions at non-toxic concentrations. Reverse transcriptase (RT) activity and p24 antigen were evaluated in culture supernatants at seven days postinfection. No effect was observed when MT-4 cells were incubated with DLE for 3 h. Whereas inhibition of HIV production was observed when MT-4 cells were pre-treated for a longer period of time. DLE inhibited p24 production and RT activity more than 50% at 0.1 m.o.i. More than 80% of inhibition was observed for all doses of DLE tested at 0.05 m.o.i. Higher viral doses (m.o.i. 0.5 and 1) were used to assess the antiviral activity of DLE fractions. Fraction Fb inhibits viral production more than 80%. Otherwise, fractions Fa and Fc did not show inhibitory effect for any viral dose used. These results indicate that DLE is able to modulate cell susceptibility to viral infection in vitro.
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PMID:Inhibition of in vitro HIV infection by dialysable leucocyte extracts. 899 55


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