Signalome-wide assessment of host cell response to hepatitis C virus
Identifieur interne : 000377 ( Main/Exploration ); précédent : 000376; suivant : 000378Signalome-wide assessment of host cell response to hepatitis C virus
Auteurs : Gholamreza Haqshenas [Australie] ; Jianmin Wu [Australie, République populaire de Chine] ; Kaylene J. Simpson [Australie] ; Roger J. Daly [Australie] ; Hans J. Netter [Australie] ; Thomas F. Baumert [France] ; Christian Doerig [Australie]Source :
- Nature Communications [ 2041-1723 ] ; 2017.
Abstract
Host cell signalling during infection with intracellular pathogens remains poorly understood. Here we report on the use of antibody microarray technology to detect variations in the expression levels and phosphorylation status of host cell signalling proteins during hepatitis C virus (HCV) replication. Following transfection with HCV RNA, the JNK and NF-κB pathways are suppressed, while the JAK/STAT5 pathway is activated; furthermore, components of the apoptosis and cell cycle control machineries are affected in the expression and/or phosphorylation status. RNAi-based hit validation identifies components of the JAK/STAT, NF-κB, MAPK and calcium-induced pathways as modulators of HCV replication. Selective chemical inhibition of one of the identified targets, the JNK activator kinase MAP4K2, does impair HCV replication. Thus this study provides a comprehensive picture of host cell pathway mobilization by HCV and uncovers potential therapeutic targets. The strategy of identifying targets for anti-infective intervention within the host cell signalome can be applied to any intracellular pathogen.
Url:
DOI: 10.1038/ncomms15158
PubMed: 28480889
PubMed Central: 5424167
Affiliations:
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Daly</name><affiliation wicri:level="1"><nlm:aff id="a7"><institution>Cancer Program, Monash Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University</institution>, Clayton Victoria 3800,<country>Australia</country></nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Netter, Hans J" sort="Netter, Hans J" uniqKey="Netter H" first="Hans J." last="Netter">Hans J. 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Baumert</name><affiliation wicri:level="1"><nlm:aff id="a9"><institution>Inserm U1110, Institut de Recherche sur les Maladies Virales et Hépatiques, Université de Strasbourg</institution>, 67091 Strasbourg,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="a10"><institution>Institut Hospitalo-Universitaire, Pôle Hépato-digestif, Hôpitaux Universitaires de Strasbourg</institution>, 67091 Strasbourg,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Doerig, Christian" sort="Doerig, Christian" uniqKey="Doerig C" first="Christian" last="Doerig">Christian Doerig</name><affiliation wicri:level="1"><nlm:aff id="a1"><institution>Infection & Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University</institution>, Clayton Victoria 3800,<country>Australia</country></nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Nature Communications</title><idno type="eISSN">2041-1723</idno><imprint><date when="2017">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Host cell signalling during infection with intracellular pathogens remains poorly understood. Here we report on the use of antibody microarray technology to detect variations in the expression levels and phosphorylation status of host cell signalling proteins during hepatitis C virus (HCV) replication. Following transfection with HCV RNA, the JNK and NF-κB pathways are suppressed, while the JAK/STAT5 pathway is activated; furthermore, components of the apoptosis and cell cycle control machineries are affected in the expression and/or phosphorylation status. RNAi-based hit validation identifies components of the JAK/STAT, NF-κB, MAPK and calcium-induced pathways as modulators of HCV replication. Selective chemical inhibition of one of the identified targets, the JNK activator kinase MAP4K2, does impair HCV replication. Thus this study provides a comprehensive picture of host cell pathway mobilization by HCV and uncovers potential therapeutic targets. The strategy of identifying targets for anti-infective intervention within the host cell signalome can be applied to any intracellular pathogen.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Mehta, S H" uniqKey="Mehta S">S. H. Mehta</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schuppan, D" uniqKey="Schuppan D">D. Schuppan</name></author><author><name sortKey="Krebs, A" uniqKey="Krebs A">A. Krebs</name></author><author><name sortKey="Bauer, M" uniqKey="Bauer M">M. Bauer</name></author><author><name sortKey="Hahn, E G" uniqKey="Hahn E">E. G. Hahn</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gower, E" uniqKey="Gower E">E. Gower</name></author><author><name sortKey="Estes, C" uniqKey="Estes C">C. Estes</name></author><author><name sortKey="Blach, S" uniqKey="Blach S">S. 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Netter</name><name sortKey="Netter, Hans J" sort="Netter, Hans J" uniqKey="Netter H" first="Hans J." last="Netter">Hans J. Netter</name><name sortKey="Simpson, Kaylene J" sort="Simpson, Kaylene J" uniqKey="Simpson K" first="Kaylene J." last="Simpson">Kaylene J. Simpson</name><name sortKey="Simpson, Kaylene J" sort="Simpson, Kaylene J" uniqKey="Simpson K" first="Kaylene J." last="Simpson">Kaylene J. Simpson</name><name sortKey="Wu, Jianmin" sort="Wu, Jianmin" uniqKey="Wu J" first="Jianmin" last="Wu">Jianmin Wu</name><name sortKey="Wu, Jianmin" sort="Wu, Jianmin" uniqKey="Wu J" first="Jianmin" last="Wu">Jianmin Wu</name></country><country name="République populaire de Chine"><noRegion><name sortKey="Wu, Jianmin" sort="Wu, Jianmin" uniqKey="Wu J" first="Jianmin" last="Wu">Jianmin Wu</name></noRegion></country><country name="France"><noRegion><name sortKey="Baumert, Thomas F" sort="Baumert, Thomas F" uniqKey="Baumert T" first="Thomas F." last="Baumert">Thomas F. Baumert</name></noRegion><name sortKey="Baumert, Thomas F" sort="Baumert, Thomas F" uniqKey="Baumert T" first="Thomas F." last="Baumert">Thomas F. Baumert</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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