FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2092244766> ?p ?o ?g. }

• W2092244766 endingPage "1462" @default.
• W2092244766 startingPage "1452" @default.
• W2092244766 abstract "Hepatitis C virus (HCV) infection is a major cause of chronic liver disease and hepatocellular carcinoma, yet fully efficacious treatments are missing. In this study, we investigated RNA interference (RNAi), a specific gene silencing process mediated by small interfering RNA (siRNA) duplexes, as an antiviral strategy against HCV. Synthetic siRNAs were designed to target conserved sequences of the HCV 5′ nontranslated region (NTR) located in a functional, stem–loop structured domain of the HCV internal ribosome entry site (IRES), which is crucial for initiation of polyprotein translation. Several siRNAs dramatically reduced or even abrogated the replication of selectable subgenomic HCV replicons upon cotransfection of human hepatoma cells with viral target and siRNAs, or upon transfection of cells supporting autonomous replication of HCV replicon with siRNAs. Importantly, three siRNAs also proved capable of strongly inhibiting virus production in cell culture. One siRNA, targeting a sequence that is highly conserved across all genotypes and forms a critical pseudoknot structure involved in translation, was identified as the most promising therapeutic candidate. These results indicate that the HCV life cycle can be efficiently blocked by using properly-designed siRNAs that target functionally important, highly conserved sequences of the HCV IRES. This finding offers a novel approach towards developing IRES-based antiviral treatment for chronic HCV infections. Hepatitis C virus (HCV) infection is a major cause of chronic liver disease and hepatocellular carcinoma, yet fully efficacious treatments are missing. In this study, we investigated RNA interference (RNAi), a specific gene silencing process mediated by small interfering RNA (siRNA) duplexes, as an antiviral strategy against HCV. Synthetic siRNAs were designed to target conserved sequences of the HCV 5′ nontranslated region (NTR) located in a functional, stem–loop structured domain of the HCV internal ribosome entry site (IRES), which is crucial for initiation of polyprotein translation. Several siRNAs dramatically reduced or even abrogated the replication of selectable subgenomic HCV replicons upon cotransfection of human hepatoma cells with viral target and siRNAs, or upon transfection of cells supporting autonomous replication of HCV replicon with siRNAs. Importantly, three siRNAs also proved capable of strongly inhibiting virus production in cell culture. One siRNA, targeting a sequence that is highly conserved across all genotypes and forms a critical pseudoknot structure involved in translation, was identified as the most promising therapeutic candidate. These results indicate that the HCV life cycle can be efficiently blocked by using properly-designed siRNAs that target functionally important, highly conserved sequences of the HCV IRES. This finding offers a novel approach towards developing IRES-based antiviral treatment for chronic HCV infections." @default.
• W2092244766 created "2016-06-24" @default.
• W2092244766 creator A5010182717 @default.
• W2092244766 creator A5022677164 @default.
• W2092244766 creator A5038988071 @default.
• W2092244766 creator A5041483008 @default.
• W2092244766 creator A5055902881 @default.
• W2092244766 creator A5061156511 @default.
• W2092244766 creator A5065268706 @default.
• W2092244766 creator A5069110978 @default.
• W2092244766 date "2007-08-01" @default.
• W2092244766 modified "2023-10-16" @default.
• W2092244766 title "Inhibition of Hepatitis C Virus Infection in Cell Culture by Small Interfering RNAs" @default.
• W2092244766 cites W1535549793 @default.
• W2092244766 cites W1542390893 @default.
• W2092244766 cites W1593744374 @default.
• W2092244766 cites W1908113512 @default.
• W2092244766 cites W1956205882 @default.
• W2092244766 cites W1966106398 @default.
• W2092244766 cites W1971643509 @default.
• W2092244766 cites W1976844675 @default.
• W2092244766 cites W1980105029 @default.
• W2092244766 cites W1988500121 @default.
• W2092244766 cites W1991902309 @default.
• W2092244766 cites W2001119248 @default.
• W2092244766 cites W2003579943 @default.
• W2092244766 cites W2006231275 @default.
• W2092244766 cites W2006447428 @default.
• W2092244766 cites W2019631541 @default.
• W2092244766 cites W2022687771 @default.
• W2092244766 cites W2023684140 @default.
• W2092244766 cites W2025254592 @default.
• W2092244766 cites W2028692573 @default.
• W2092244766 cites W2030111552 @default.
• W2092244766 cites W2037342510 @default.
• W2092244766 cites W2047165821 @default.
• W2092244766 cites W2047937065 @default.
• W2092244766 cites W2069573487 @default.
• W2092244766 cites W2069608350 @default.
• W2092244766 cites W2071662566 @default.
• W2092244766 cites W2072697431 @default.
• W2092244766 cites W2100796404 @default.
• W2092244766 cites W2102068103 @default.
• W2092244766 cites W2109136664 @default.
• W2092244766 cites W2112930049 @default.
• W2092244766 cites W2113154128 @default.
• W2092244766 cites W2116424844 @default.
• W2092244766 cites W2122987848 @default.
• W2092244766 cites W2125057438 @default.
• W2092244766 cites W2127444976 @default.
• W2092244766 cites W2128212057 @default.
• W2092244766 cites W2132209533 @default.
• W2092244766 cites W2133100251 @default.
• W2092244766 cites W2136177706 @default.
• W2092244766 cites W2139871850 @default.
• W2092244766 cites W2140091023 @default.
• W2092244766 cites W2140440263 @default.
• W2092244766 cites W2140518449 @default.
• W2092244766 cites W2140654254 @default.
• W2092244766 cites W2150742206 @default.
• W2092244766 cites W2151437059 @default.
• W2092244766 cites W2151898297 @default.
• W2092244766 cites W2160390885 @default.
• W2092244766 cites W2162714406 @default.
• W2092244766 cites W2166802510 @default.
• W2092244766 cites W4230988890 @default.
• W2092244766 cites W4376849510 @default.
• W2092244766 doi "https://doi.org/10.1038/sj.mt.6300186" @default.
• W2092244766 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7106008" @default.
• W2092244766 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17505476" @default.
• W2092244766 hasPublicationYear "2007" @default.
• W2092244766 type Work @default.
• W2092244766 sameAs 2092244766 @default.
• W2092244766 citedByCount "48" @default.
• W2092244766 countsByYear W20922447662012 @default.
• W2092244766 countsByYear W20922447662013 @default.
• W2092244766 countsByYear W20922447662014 @default.
• W2092244766 countsByYear W20922447662015 @default.
• W2092244766 countsByYear W20922447662016 @default.
• W2092244766 countsByYear W20922447662017 @default.
• W2092244766 countsByYear W20922447662021 @default.
• W2092244766 crossrefType "journal-article" @default.
• W2092244766 hasAuthorship W2092244766A5010182717 @default.
• W2092244766 hasAuthorship W2092244766A5022677164 @default.
• W2092244766 hasAuthorship W2092244766A5038988071 @default.
• W2092244766 hasAuthorship W2092244766A5041483008 @default.
• W2092244766 hasAuthorship W2092244766A5055902881 @default.
• W2092244766 hasAuthorship W2092244766A5061156511 @default.
• W2092244766 hasAuthorship W2092244766A5065268706 @default.
• W2092244766 hasAuthorship W2092244766A5069110978 @default.
• W2092244766 hasBestOaLocation W20922447661 @default.
• W2092244766 hasConcept C104317684 @default.
• W2092244766 hasConcept C119056186 @default.
• W2092244766 hasConcept C159047783 @default.
• W2092244766 hasConcept C166703698 @default.
• W2092244766 hasConcept C18103114 @default.
• W2092244766 hasConcept C189819185 @default.
• W2092244766 hasConcept C2191507 @default.

• next