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NS5B

About: NS5B is a research topic. Over the lifetime, 1314 publications have been published within this topic receiving 59534 citations.


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Journal ArticleDOI
TL;DR: The results suggested that the combination of alpha‐IFN 2b and ribavirin might induce mutations, and inhibit HCV RNA synthesis in hepatocytes to a greater extent than Ribavirin monotherapy.
Abstract: Hepatitis C virus (HCV) infection is a major problem throughout the world Combination therapy of interferon (IFN) and ribavirin is the best treatment for eradication at present, but the mechanism is not completely understood We used the HCV replicon system to investigate this mechanism The effects of six drugs (UDCA, glycyrrhizin, TJ-9, bezafibrate, ribavirin, and alpha-IFN 2b) on HCV subgenomic RNA (genotype 1b, NS5B 415Y) were examined by reverse transcription polymerase chain reaction, cloning and sequencing The HCV replication was inhibited by alpha-IFN 2b (739-132% at 10 U/mL, 329-612% at 100 U/mL, 13-486% at 1000 U/mL) and by ribavirin (436-139% at 100 microg/mL), but not by the other drugs at 24-72 h after treatment Furthermore, the combination treatment was superior to IFN monotherapy and to ribavirin monotherapy at 72 h post-treatment Sequence analyses of the double-stranded RNA-activated protein kinase (PKR)-binding domain and flanking regions within the HCV NS5A region revealed that the total numbers of substitutions caused by ribavirin (n = 36) or combination treatment (n = 57) were more than those of IFN alone (n = 5) and controls (n = 6) The HCV replicon system is the most efficient system for HCV replication and is an excellent choice for testing anti-HCV drugs and disinfectants Our results further suggested that the combination of alpha-IFN 2b and ribavirin might induce mutations, and inhibit HCV RNA synthesis in hepatocytes to a greater extent than ribavirin monotherapy

59 citations

Journal ArticleDOI
TL;DR: The molecular targets and chemical structures of drugs used in HCV treatment are reviewed andications and contraindications for anti-HCV drugs are also discussed together with application regimens.

59 citations

Journal ArticleDOI
05 Feb 2011-Virology
TL;DR: Comparative proteome analyses of HCV replication complex (RC)-rich membrane fractions prepared from cells harboring genome-length bicistronic HCV RNA suggest that recruitment of the chaperonin by the viral nonstructural proteins to the RC, which potentially facilitate folding of the RC component(s) into the mature active form, may be important for efficient replication of the HCV genome.

59 citations

Journal ArticleDOI
TL;DR: The results suggest that ns4 and ns5a are not essential for viral replication in tissue culture cells, and thus join gene 2 and the hemagglutinin-esterase gene as nonessential viral genes in MHV.
Abstract: Genes 4 and 5 of mouse hepatitis virus (MHV) are known to encode nonstructural proteins ns4, ns5a, and ns5b, whose function is unknown. In this study, we demonstrated that one of the MHV strains, MHV-S, did not synthesize mRNA 4 and made a smaller mRNA 5. Sequence analysis showed that the transcription initiation site for gene 4 of MHV-S was mutated from the consensus UCUAAAC to UUUAAAC, consistent with the idea that mutations in this region abolish mRNA synthesis. Furthermore, within gene 5 there were deletions totaling 307 nucleotides which deleted almost all of open reading frame 5a, but preserved open reading frame 5b of gene 5. Comparison of the growth of MHV-S with other MHV strains in DBT cells revealed no significant growth defect in MHV-S. These results suggest that ns4 and ns5a are not essential for viral replication in tissue culture cells, and thus join gene 2 and the hemagglutinin-esterase (HE) gene as nonessential viral genes in MHV.

59 citations

Journal ArticleDOI
TL;DR: It is proposed that this compound shares critical common features for activity with alpha,gamma-diketoacids inhibitors previously discovered by this group, which will provide an improved basis for structure-based ligand design.

59 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202310
202258
202128
202033
201943
201842