High-throughput approaches to unravel hepatitis C virus-host interactions
Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therap...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Colpitts, Che C. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016transfer abstract |
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| Umfang: |
7 |
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| Übergeordnetes Werk: |
Enthalten in: AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells - Shimura, Tsutomu ELSEVIER, 2014, an international journal of molecular and cellular virology, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:218 ; year:2016 ; day:15 ; month:06 ; pages:18-24 ; extent:7 |
| Links: |
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| DOI / URN: |
10.1016/j.virusres.2015.09.013 |
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| 520 | |a Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. | ||
| 520 | |a Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. | ||
| 650 | 7 | |a Systems biology |2 Elsevier | |
| 650 | 7 | |a HCV pathogenesis |2 Elsevier | |
| 650 | 7 | |a Hepatitis C virus |2 Elsevier | |
| 650 | 7 | |a Virus-host interactions |2 Elsevier | |
| 700 | 1 | |a El-Saghire, Hussein |4 oth | |
| 700 | 1 | |a Pochet, Nathalie |4 oth | |
| 700 | 1 | |a Schuster, Catherine |4 oth | |
| 700 | 1 | |a Baumert, Thomas F. |4 oth | |
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10.1016/j.virusres.2015.09.013 doi GBVA2016005000027.pica (DE-627)ELV029577306 (ELSEVIER)S0168-1702(15)30069-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 570 540 VZ Colpitts, Che C. verfasserin aut High-throughput approaches to unravel hepatitis C virus-host interactions 2016transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. Systems biology Elsevier HCV pathogenesis Elsevier Hepatitis C virus Elsevier Virus-host interactions Elsevier El-Saghire, Hussein oth Pochet, Nathalie oth Schuster, Catherine oth Baumert, Thomas F. oth Enthalten in Elsevier Science Shimura, Tsutomu ELSEVIER AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells 2014 an international journal of molecular and cellular virology Amsterdam [u.a.] (DE-627)ELV012046744 volume:218 year:2016 day:15 month:06 pages:18-24 extent:7 https://doi.org/10.1016/j.virusres.2015.09.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA AR 218 2016 15 0615 18-24 7 045F 610 |
| spelling |
10.1016/j.virusres.2015.09.013 doi GBVA2016005000027.pica (DE-627)ELV029577306 (ELSEVIER)S0168-1702(15)30069-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 570 540 VZ Colpitts, Che C. verfasserin aut High-throughput approaches to unravel hepatitis C virus-host interactions 2016transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. Systems biology Elsevier HCV pathogenesis Elsevier Hepatitis C virus Elsevier Virus-host interactions Elsevier El-Saghire, Hussein oth Pochet, Nathalie oth Schuster, Catherine oth Baumert, Thomas F. oth Enthalten in Elsevier Science Shimura, Tsutomu ELSEVIER AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells 2014 an international journal of molecular and cellular virology Amsterdam [u.a.] (DE-627)ELV012046744 volume:218 year:2016 day:15 month:06 pages:18-24 extent:7 https://doi.org/10.1016/j.virusres.2015.09.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA AR 218 2016 15 0615 18-24 7 045F 610 |
| allfields_unstemmed |
10.1016/j.virusres.2015.09.013 doi GBVA2016005000027.pica (DE-627)ELV029577306 (ELSEVIER)S0168-1702(15)30069-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 570 540 VZ Colpitts, Che C. verfasserin aut High-throughput approaches to unravel hepatitis C virus-host interactions 2016transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. Systems biology Elsevier HCV pathogenesis Elsevier Hepatitis C virus Elsevier Virus-host interactions Elsevier El-Saghire, Hussein oth Pochet, Nathalie oth Schuster, Catherine oth Baumert, Thomas F. oth Enthalten in Elsevier Science Shimura, Tsutomu ELSEVIER AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells 2014 an international journal of molecular and cellular virology Amsterdam [u.a.] (DE-627)ELV012046744 volume:218 year:2016 day:15 month:06 pages:18-24 extent:7 https://doi.org/10.1016/j.virusres.2015.09.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA AR 218 2016 15 0615 18-24 7 045F 610 |
| allfieldsGer |
10.1016/j.virusres.2015.09.013 doi GBVA2016005000027.pica (DE-627)ELV029577306 (ELSEVIER)S0168-1702(15)30069-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 570 540 VZ Colpitts, Che C. verfasserin aut High-throughput approaches to unravel hepatitis C virus-host interactions 2016transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. Systems biology Elsevier HCV pathogenesis Elsevier Hepatitis C virus Elsevier Virus-host interactions Elsevier El-Saghire, Hussein oth Pochet, Nathalie oth Schuster, Catherine oth Baumert, Thomas F. oth Enthalten in Elsevier Science Shimura, Tsutomu ELSEVIER AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells 2014 an international journal of molecular and cellular virology Amsterdam [u.a.] (DE-627)ELV012046744 volume:218 year:2016 day:15 month:06 pages:18-24 extent:7 https://doi.org/10.1016/j.virusres.2015.09.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA AR 218 2016 15 0615 18-24 7 045F 610 |
| allfieldsSound |
10.1016/j.virusres.2015.09.013 doi GBVA2016005000027.pica (DE-627)ELV029577306 (ELSEVIER)S0168-1702(15)30069-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 570 540 VZ Colpitts, Che C. verfasserin aut High-throughput approaches to unravel hepatitis C virus-host interactions 2016transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. Systems biology Elsevier HCV pathogenesis Elsevier Hepatitis C virus Elsevier Virus-host interactions Elsevier El-Saghire, Hussein oth Pochet, Nathalie oth Schuster, Catherine oth Baumert, Thomas F. oth Enthalten in Elsevier Science Shimura, Tsutomu ELSEVIER AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells 2014 an international journal of molecular and cellular virology Amsterdam [u.a.] (DE-627)ELV012046744 volume:218 year:2016 day:15 month:06 pages:18-24 extent:7 https://doi.org/10.1016/j.virusres.2015.09.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA AR 218 2016 15 0615 18-24 7 045F 610 |
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Enthalten in AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells Amsterdam [u.a.] volume:218 year:2016 day:15 month:06 pages:18-24 extent:7 |
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Enthalten in AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells Amsterdam [u.a.] volume:218 year:2016 day:15 month:06 pages:18-24 extent:7 |
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AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells |
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Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. |
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Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. |
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Hepatitis C virus (HCV) remains a major global health burden, with more than 130 million individuals chronically infected and at risk for the development of hepatocellular carcinoma (HCC). The recent clinical licensing of direct-acting antivirals enables viral cure. However, limited access to therapy and treatment failure in patient subgroups warrants a continuing effort to develop complementary antiviral strategies. Furthermore, once fibrosis is established, curing HCV infection does not eliminate the risk for HCC. High-throughput approaches and screens have enabled the investigation of virus-host interactions on a genome-wide scale. Gain- and loss-of-function screens have identified essential host-dependency factors in the HCV viral life cycle, such as host cell entry factors or regulatory factors for viral replication and assembly. Network analyses of systems-scale data sets provided a comprehensive view of the cellular state following HCV infection, thus improving our understanding of the virus-induced responses of the target cell. Interactome, metabolomics and gene expression studies identified dysregulated cellular processes potentially contributing to HCV pathogenesis and HCC. Drug screens using chemical libraries led to the discovery of novel antivirals. Here, we review the contribution of high-throughput approaches for the investigation of virus-host interactions, viral pathogenesis and drug discovery. |
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