Identification of type I and type II interferon‐induced effectors controlling hepatitis C virus replication
Identifieur interne : 001E76 ( Main/Exploration ); précédent : 001E75; suivant : 001E77Identification of type I and type II interferon‐induced effectors controlling hepatitis C virus replication
Auteurs : Philippe Metz [Allemagne] ; Eva Dazert [Allemagne, Suisse] ; Alessia Ruggieri [Allemagne] ; Johanna Mazur [Allemagne] ; Lars Kaderali [Allemagne] ; Artur Kaul [Allemagne] ; Ulf Zeuge [Allemagne, Suisse] ; Marc P. Windisch [Allemagne, Corée du Sud] ; Martin Trippler [Allemagne] ; Volker Lohmann [Allemagne] ; Marco Binder [Allemagne] ; Michael Frese [Allemagne, Australie] ; Ralf Bartenschlager [Allemagne]Source :
- Hepatology [ 0270-9139 ] ; 2012-12.
English descriptors
- Teeft :
- Antiviral, Antiviral activity, Antiviral effect, Antiviral response, Antiviral state, Assay, Bartenschlager, Candidate isgs, Cell culture, Cell pools stably overexpressing, Cell viability, Chronic hepatitis, Combinatorial, Con1 replicons, Concerted action, Cytokine, Effector, Error bars, Hepatitis, Hepatology, Ifit3, Ifit3 protein, Ifitm1, Independent experiments, Individual isgs, Interferon, Interferon cytokine, Isgs, Kinetics, Life technologies, Liver diseases, Luciferase, Luciferase activity, Luciferase assay, Luciferase expression, Luciferase reporter replicon, Luciferase values, Metz, Molecular virology, Mrna, Mrna levels, Multiple isgs, Negative control, Nitric oxide, Nitric oxide synthase, Nontargeting sirna, Nos2, Other isgs, Overexpression, Phospholipid scramblase, Plain medium, Pleiotropic effects, Plscr1, Positive controls, Present address, Primary screen, Protein family, Protein kinase, Replication, Replication inhibition, Replicon, Replicon cells, Restriction factors, Screening approach, Screening assay, Several isgs, Sirna, Sirnas, Standard deviations, Subgenomic, Subgenomic replicons, Substantial overlap, Synergistic effects, Transcription factors, Tripartite motif, Triplicate measurements, Validation screen, Viral, Viral hepat, Viral replication, Virus infection, Virus replication, Virus rnas.
Abstract
Persistent infection with hepatitis C virus (HCV) can lead to chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. All current therapies of hepatitis C include interferon‐alpha (IFN‐α). Moreover, IFN‐gamma (IFN‐γ), the only type II IFN, strongly inhibits HCV replication in vitro and is the primary mediator of HCV‐specific antiviral T‐cell responses. However, for both cytokines the precise set of effector protein(s) responsible for replication inhibition is not known. The aim of this study was the identification of IFN‐α and IFN‐γ stimulated genes (ISGs) responsible for controlling HCV replication. We devised an RNA interference (RNAi)‐based “gain of function” screen and identified, in addition to known ISGs earlier reported to suppress HCV replication, several new ones with proven antiviral activity. These include IFIT3 (IFN‐induced protein with tetratricopeptide repeats 3), TRIM14 (tripartite motif containing 14), PLSCR1 (phospholipid scramblase 1), and NOS2 (nitric oxide synthase 2, inducible). All ISGs identified in this study were up‐regulated both by IFN‐α and IFN‐γ, demonstrating a substantial overlap of HCV‐specific effectors induced by either cytokine. Nevertheless, some ISGs were more specific for IFN‐α or IFN‐γ, which was most pronounced in case of PLSCR1 and NOS2 that were identified as main effectors of IFN‐γ‐mediated anti‐HCV activity. Combinatorial knockdowns of ISGs suggest additive or synergistic effects demonstrating that with either IFN, inhibition of HCV replication is caused by the combined action of multiple ISGs. Conclusion: Our study identifies a number of novel ISGs contributing to the suppression of HCV replication by type I and type II IFN. We demonstrate a substantial overlap of antiviral programs triggered by either cytokine and show that suppression of HCV replication is mediated by the concerted action of multiple effectors. (HEPATOLOGY 2012;56:2082–2093)
Url:
DOI: 10.1002/hep.25908
Affiliations:
- Allemagne, Australie, Corée du Sud, Suisse
- Bade-Wurtemberg, Bavière, District de Dresde, District de Karlsruhe, District de Moyenne-Franconie, Saxe (Land)
- Dresde, Erlangen, Heidelberg
Links toward previous steps (curation, corpus...)
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Le document en format XML
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uniqKey="Ruggieri A" first="Alessia" last="Ruggieri">Alessia Ruggieri</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Molecular Virology, University of Heidelberg</wicri:regionArea><wicri:noRegion>University of Heidelberg</wicri:noRegion><wicri:noRegion>University of Heidelberg</wicri:noRegion></affiliation></author><author><name sortKey="Mazur, Johanna" sort="Mazur, Johanna" uniqKey="Mazur J" first="Johanna" last="Mazur">Johanna Mazur</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Bioquant, Viroquant Research Group Modeling, University of Heidelberg</wicri:regionArea><wicri:noRegion>University of Heidelberg</wicri:noRegion><wicri:noRegion>University of Heidelberg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Current Address: Institute of Medical Biometry, Epidemiology and Informatics, University of Mainz</wicri:regionArea><wicri:noRegion>University of Mainz</wicri:noRegion><wicri:noRegion>University of Mainz</wicri:noRegion></affiliation></author><author><name sortKey="Kaderali, Lars" sort="Kaderali, Lars" uniqKey="Kaderali L" first="Lars" last="Kaderali">Lars Kaderali</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Bioquant, Viroquant Research Group Modeling, University of Heidelberg</wicri:regionArea><wicri:noRegion>University of Heidelberg</wicri:noRegion><wicri:noRegion>University of Heidelberg</wicri:noRegion></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Current Address: Institute for Medical Informatics and Biometry, Dresden</wicri:regionArea><placeName><region type="land" nuts="1">Saxe (Land)</region><region type="district" nuts="2">District de Dresde</region><settlement type="city">Dresde</settlement></placeName></affiliation></author><author><name sortKey="Kaul, Artur" sort="Kaul, Artur" uniqKey="Kaul A" first="Artur" last="Kaul">Artur Kaul</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Molecular Virology, University of Heidelberg</wicri:regionArea><wicri:noRegion>University of Heidelberg</wicri:noRegion><wicri:noRegion>University of Heidelberg</wicri:noRegion></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Current Address: ViroLogik GmbH, Erlangen</wicri:regionArea><placeName><settlement type="city">Erlangen</settlement><region type="land" nuts="1">Bavière</region><region type="district" nuts="2">District de Moyenne-Franconie</region></placeName></affiliation></author><author><name sortKey="Zeuge, Ulf" sort="Zeuge, Ulf" uniqKey="Zeuge U" first="Ulf" last="Zeuge">Ulf Zeuge</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Molecular Virology, University of 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Essen</wicri:noRegion><wicri:noRegion>University Hospital Essen</wicri:noRegion></affiliation></author><author><name sortKey="Lohmann, Volker" sort="Lohmann, Volker" uniqKey="Lohmann V" first="Volker" last="Lohmann">Volker Lohmann</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Molecular Virology, University of Heidelberg</wicri:regionArea><wicri:noRegion>University of Heidelberg</wicri:noRegion><wicri:noRegion>University of Heidelberg</wicri:noRegion></affiliation></author><author><name sortKey="Binder, Marco" sort="Binder, Marco" uniqKey="Binder M" first="Marco" last="Binder">Marco Binder</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Molecular Virology, University of Heidelberg</wicri:regionArea><wicri:noRegion>University of Heidelberg</wicri:noRegion><wicri:noRegion>University of Heidelberg</wicri:noRegion></affiliation></author><author><name sortKey="Frese, Michael" sort="Frese, Michael" uniqKey="Frese M" first="Michael" last="Frese">Michael Frese</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Molecular Virology, University of Heidelberg</wicri:regionArea><wicri:noRegion>University of Heidelberg</wicri:noRegion><wicri:noRegion>University of Heidelberg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Current Address: Faculty of Applied Science, University of Canberra, ACT 2601</wicri:regionArea><wicri:noRegion>ACT 2601</wicri:noRegion></affiliation></author><author><name sortKey="Bartenschlager, Ralf" sort="Bartenschlager, Ralf" uniqKey="Bartenschlager R" first="Ralf" last="Bartenschlager">Ralf Bartenschlager</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Molecular Virology, University of Heidelberg</wicri:regionArea><wicri:noRegion>University of Heidelberg</wicri:noRegion><wicri:noRegion>University of Heidelberg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Allemagne</country></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Correspondence address: Im Neuenheimer Feld 345, 69124 Heidelberg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Karlsruhe</region><settlement type="city">Heidelberg</settlement></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Hepatology</title><title level="j" type="alt">HEPATOLOGY</title><idno type="ISSN">0270-9139</idno><idno type="eISSN">1527-3350</idno><imprint><biblScope unit="vol">56</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="2082">2082</biblScope><biblScope unit="page" to="2093">2093</biblScope><biblScope unit="page-count">12</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2012-12">2012-12</date></imprint><idno type="ISSN">0270-9139</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0270-9139</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Antiviral</term><term>Antiviral activity</term><term>Antiviral effect</term><term>Antiviral response</term><term>Antiviral state</term><term>Assay</term><term>Bartenschlager</term><term>Candidate isgs</term><term>Cell culture</term><term>Cell pools stably overexpressing</term><term>Cell viability</term><term>Chronic hepatitis</term><term>Combinatorial</term><term>Con1 replicons</term><term>Concerted action</term><term>Cytokine</term><term>Effector</term><term>Error bars</term><term>Hepatitis</term><term>Hepatology</term><term>Ifit3</term><term>Ifit3 protein</term><term>Ifitm1</term><term>Independent experiments</term><term>Individual isgs</term><term>Interferon</term><term>Interferon cytokine</term><term>Isgs</term><term>Kinetics</term><term>Life technologies</term><term>Liver diseases</term><term>Luciferase</term><term>Luciferase activity</term><term>Luciferase assay</term><term>Luciferase expression</term><term>Luciferase reporter replicon</term><term>Luciferase values</term><term>Metz</term><term>Molecular virology</term><term>Mrna</term><term>Mrna levels</term><term>Multiple isgs</term><term>Negative control</term><term>Nitric oxide</term><term>Nitric oxide synthase</term><term>Nontargeting sirna</term><term>Nos2</term><term>Other isgs</term><term>Overexpression</term><term>Phospholipid scramblase</term><term>Plain medium</term><term>Pleiotropic effects</term><term>Plscr1</term><term>Positive controls</term><term>Present address</term><term>Primary screen</term><term>Protein family</term><term>Protein kinase</term><term>Replication</term><term>Replication inhibition</term><term>Replicon</term><term>Replicon cells</term><term>Restriction factors</term><term>Screening approach</term><term>Screening assay</term><term>Several isgs</term><term>Sirna</term><term>Sirnas</term><term>Standard deviations</term><term>Subgenomic</term><term>Subgenomic replicons</term><term>Substantial overlap</term><term>Synergistic effects</term><term>Transcription factors</term><term>Tripartite motif</term><term>Triplicate measurements</term><term>Validation screen</term><term>Viral</term><term>Viral hepat</term><term>Viral replication</term><term>Virus infection</term><term>Virus replication</term><term>Virus rnas</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Persistent infection with hepatitis C virus (HCV) can lead to chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. All current therapies of hepatitis C include interferon‐alpha (IFN‐α). Moreover, IFN‐gamma (IFN‐γ), the only type II IFN, strongly inhibits HCV replication in vitro and is the primary mediator of HCV‐specific antiviral T‐cell responses. However, for both cytokines the precise set of effector protein(s) responsible for replication inhibition is not known. The aim of this study was the identification of IFN‐α and IFN‐γ stimulated genes (ISGs) responsible for controlling HCV replication. We devised an RNA interference (RNAi)‐based “gain of function” screen and identified, in addition to known ISGs earlier reported to suppress HCV replication, several new ones with proven antiviral activity. These include IFIT3 (IFN‐induced protein with tetratricopeptide repeats 3), TRIM14 (tripartite motif containing 14), PLSCR1 (phospholipid scramblase 1), and NOS2 (nitric oxide synthase 2, inducible). All ISGs identified in this study were up‐regulated both by IFN‐α and IFN‐γ, demonstrating a substantial overlap of HCV‐specific effectors induced by either cytokine. Nevertheless, some ISGs were more specific for IFN‐α or IFN‐γ, which was most pronounced in case of PLSCR1 and NOS2 that were identified as main effectors of IFN‐γ‐mediated anti‐HCV activity. Combinatorial knockdowns of ISGs suggest additive or synergistic effects demonstrating that with either IFN, inhibition of HCV replication is caused by the combined action of multiple ISGs. Conclusion: Our study identifies a number of novel ISGs contributing to the suppression of HCV replication by type I and type II IFN. We demonstrate a substantial overlap of antiviral programs triggered by either cytokine and show that suppression of HCV replication is mediated by the concerted action of multiple effectors. (HEPATOLOGY 2012;56:2082–2093)</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Australie</li><li>Corée du Sud</li><li>Suisse</li></country><region><li>Bade-Wurtemberg</li><li>Bavière</li><li>District de Dresde</li><li>District de Karlsruhe</li><li>District de Moyenne-Franconie</li><li>Saxe (Land)</li></region><settlement><li>Dresde</li><li>Erlangen</li><li>Heidelberg</li></settlement></list><tree><country name="Allemagne"><noRegion><name sortKey="Metz, Philippe" sort="Metz, Philippe" uniqKey="Metz P" first="Philippe" last="Metz">Philippe Metz</name></noRegion><name sortKey="Bartenschlager, Ralf" sort="Bartenschlager, Ralf" uniqKey="Bartenschlager R" first="Ralf" last="Bartenschlager">Ralf Bartenschlager</name><name sortKey="Bartenschlager, Ralf" sort="Bartenschlager, Ralf" uniqKey="Bartenschlager R" first="Ralf" last="Bartenschlager">Ralf Bartenschlager</name><name sortKey="Bartenschlager, Ralf" sort="Bartenschlager, Ralf" uniqKey="Bartenschlager R" first="Ralf" last="Bartenschlager">Ralf Bartenschlager</name><name sortKey="Binder, Marco" sort="Binder, Marco" uniqKey="Binder M" first="Marco" last="Binder">Marco Binder</name><name sortKey="Dazert, Eva" sort="Dazert, Eva" uniqKey="Dazert E" first="Eva" last="Dazert">Eva Dazert</name><name sortKey="Frese, Michael" sort="Frese, Michael" uniqKey="Frese M" first="Michael" last="Frese">Michael Frese</name><name sortKey="Kaderali, Lars" sort="Kaderali, Lars" uniqKey="Kaderali L" first="Lars" last="Kaderali">Lars Kaderali</name><name sortKey="Kaderali, Lars" sort="Kaderali, Lars" uniqKey="Kaderali L" first="Lars" last="Kaderali">Lars Kaderali</name><name sortKey="Kaul, Artur" sort="Kaul, Artur" uniqKey="Kaul A" first="Artur" last="Kaul">Artur Kaul</name><name sortKey="Kaul, Artur" sort="Kaul, Artur" uniqKey="Kaul A" first="Artur" last="Kaul">Artur Kaul</name><name sortKey="Lohmann, Volker" sort="Lohmann, Volker" uniqKey="Lohmann V" first="Volker" last="Lohmann">Volker Lohmann</name><name sortKey="Mazur, Johanna" sort="Mazur, Johanna" uniqKey="Mazur J" first="Johanna" last="Mazur">Johanna Mazur</name><name sortKey="Mazur, Johanna" sort="Mazur, Johanna" uniqKey="Mazur J" first="Johanna" last="Mazur">Johanna Mazur</name><name sortKey="Ruggieri, Alessia" sort="Ruggieri, Alessia" uniqKey="Ruggieri A" first="Alessia" last="Ruggieri">Alessia Ruggieri</name><name sortKey="Trippler, Martin" sort="Trippler, Martin" uniqKey="Trippler M" first="Martin" last="Trippler">Martin Trippler</name><name sortKey="Windisch, Marc P" sort="Windisch, Marc P" uniqKey="Windisch M" first="Marc P." last="Windisch">Marc P. Windisch</name><name sortKey="Zeuge, Ulf" sort="Zeuge, Ulf" uniqKey="Zeuge U" first="Ulf" last="Zeuge">Ulf Zeuge</name></country><country name="Suisse"><noRegion><name sortKey="Dazert, Eva" sort="Dazert, Eva" uniqKey="Dazert E" first="Eva" last="Dazert">Eva Dazert</name></noRegion><name sortKey="Zeuge, Ulf" sort="Zeuge, Ulf" uniqKey="Zeuge U" first="Ulf" last="Zeuge">Ulf Zeuge</name></country><country name="Corée du Sud"><noRegion><name sortKey="Windisch, Marc P" sort="Windisch, Marc P" uniqKey="Windisch M" first="Marc P." last="Windisch">Marc P. Windisch</name></noRegion></country><country name="Australie"><noRegion><name sortKey="Frese, Michael" sort="Frese, Michael" uniqKey="Frese M" first="Michael" last="Frese">Michael Frese</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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