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
Autor*in: |
Colpitts, Che C. [verfasserIn] |
---|
Format: |
E-Artikel |
---|---|
Sprache: |
Englisch |
Erschienen: |
2016transfer abstract |
---|
Schlagwörter: |
---|
Umfang: |
7 |
---|
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.] |
---|---|
Übergeordnetes Werk: |
volume:218 ; year:2016 ; day:15 ; month:06 ; pages:18-24 ; extent:7 |
Links: |
---|
DOI / URN: |
10.1016/j.virusres.2015.09.013 |
---|
Katalog-ID: |
ELV029577306 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | ELV029577306 | ||
003 | DE-627 | ||
005 | 20230625174654.0 | ||
007 | cr uuu---uuuuu | ||
008 | 180603s2016 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1016/j.virusres.2015.09.013 |2 doi | |
028 | 5 | 2 | |a GBVA2016005000027.pica |
035 | |a (DE-627)ELV029577306 | ||
035 | |a (ELSEVIER)S0168-1702(15)30069-1 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
082 | 0 | |a 610 | |
082 | 0 | 4 | |a 610 |q DE-600 |
082 | 0 | 4 | |a 610 |q VZ |
082 | 0 | 4 | |a 570 |a 540 |q VZ |
100 | 1 | |a Colpitts, Che C. |e verfasserin |4 aut | |
245 | 1 | 0 | |a High-throughput approaches to unravel hepatitis C virus-host interactions |
264 | 1 | |c 2016transfer abstract | |
300 | |a 7 | ||
336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
337 | |a nicht spezifiziert |b z |2 rdamedia | ||
338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
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 | |
773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Shimura, Tsutomu ELSEVIER |t AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells |d 2014 |d an international journal of molecular and cellular virology |g Amsterdam [u.a.] |w (DE-627)ELV012046744 |
773 | 1 | 8 | |g volume:218 |g year:2016 |g day:15 |g month:06 |g pages:18-24 |g extent:7 |
856 | 4 | 0 | |u https://doi.org/10.1016/j.virusres.2015.09.013 |3 Volltext |
912 | |a GBV_USEFLAG_U | ||
912 | |a GBV_ELV | ||
912 | |a SYSFLAG_U | ||
912 | |a SSG-OLC-PHA | ||
951 | |a AR | ||
952 | |d 218 |j 2016 |b 15 |c 0615 |h 18-24 |g 7 | ||
953 | |2 045F |a 610 |
author_variant |
c c c cc ccc |
---|---|
matchkey_str |
colpittschecelsaghirehusseinpochetnathal:2016----:ihhogptprahsonaehpttsvrs |
hierarchy_sort_str |
2016transfer abstract |
publishDate |
2016 |
allfields |
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 |
language |
English |
source |
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 |
sourceStr |
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 |
format_phy_str_mv |
Article |
institution |
findex.gbv.de |
topic_facet |
Systems biology HCV pathogenesis Hepatitis C virus Virus-host interactions |
dewey-raw |
610 |
isfreeaccess_bool |
false |
container_title |
AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells |
authorswithroles_txt_mv |
Colpitts, Che C. @@aut@@ El-Saghire, Hussein @@oth@@ Pochet, Nathalie @@oth@@ Schuster, Catherine @@oth@@ Baumert, Thomas F. @@oth@@ |
publishDateDaySort_date |
2016-01-15T00:00:00Z |
hierarchy_top_id |
ELV012046744 |
dewey-sort |
3610 |
id |
ELV029577306 |
language_de |
englisch |
fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV029577306</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625174654.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2016 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.virusres.2015.09.013</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2016005000027.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV029577306</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0168-1702(15)30069-1</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="a">540</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Colpitts, Che C.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">High-throughput approaches to unravel hepatitis C virus-host interactions</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">7</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Systems biology</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HCV pathogenesis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Hepatitis C virus</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Virus-host interactions</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">El-Saghire, Hussein</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pochet, Nathalie</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schuster, Catherine</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Baumert, Thomas F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Shimura, Tsutomu ELSEVIER</subfield><subfield code="t">AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells</subfield><subfield code="d">2014</subfield><subfield code="d">an international journal of molecular and cellular virology</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV012046744</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:218</subfield><subfield code="g">year:2016</subfield><subfield code="g">day:15</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:18-24</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.virusres.2015.09.013</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">218</subfield><subfield code="j">2016</subfield><subfield code="b">15</subfield><subfield code="c">0615</subfield><subfield code="h">18-24</subfield><subfield code="g">7</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
author |
Colpitts, Che C. |
spellingShingle |
Colpitts, Che C. ddc 610 ddc 570 Elsevier Systems biology Elsevier HCV pathogenesis Elsevier Hepatitis C virus Elsevier Virus-host interactions High-throughput approaches to unravel hepatitis C virus-host interactions |
authorStr |
Colpitts, Che C. |
ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV012046744 |
format |
electronic Article |
dewey-ones |
610 - Medicine & health 570 - Life sciences; biology 540 - Chemistry & allied sciences |
delete_txt_mv |
keep |
author_role |
aut |
collection |
elsevier |
remote_str |
true |
illustrated |
Not Illustrated |
topic_title |
610 610 DE-600 610 VZ 570 540 VZ High-throughput approaches to unravel hepatitis C virus-host interactions Systems biology Elsevier HCV pathogenesis Elsevier Hepatitis C virus Elsevier Virus-host interactions Elsevier |
topic |
ddc 610 ddc 570 Elsevier Systems biology Elsevier HCV pathogenesis Elsevier Hepatitis C virus Elsevier Virus-host interactions |
topic_unstemmed |
ddc 610 ddc 570 Elsevier Systems biology Elsevier HCV pathogenesis Elsevier Hepatitis C virus Elsevier Virus-host interactions |
topic_browse |
ddc 610 ddc 570 Elsevier Systems biology Elsevier HCV pathogenesis Elsevier Hepatitis C virus Elsevier Virus-host interactions |
format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
format_main_str_mv |
Text Zeitschrift/Artikel |
carriertype_str_mv |
zu |
author2_variant |
h e s hes n p np c s cs t f b tf tfb |
hierarchy_parent_title |
AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells |
hierarchy_parent_id |
ELV012046744 |
dewey-tens |
610 - Medicine & health 570 - Life sciences; biology 540 - Chemistry |
hierarchy_top_title |
AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells |
isfreeaccess_txt |
false |
familylinks_str_mv |
(DE-627)ELV012046744 |
title |
High-throughput approaches to unravel hepatitis C virus-host interactions |
ctrlnum |
(DE-627)ELV029577306 (ELSEVIER)S0168-1702(15)30069-1 |
title_full |
High-throughput approaches to unravel hepatitis C virus-host interactions |
author_sort |
Colpitts, Che C. |
journal |
AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells |
journalStr |
AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells |
lang_code |
eng |
isOA_bool |
false |
dewey-hundreds |
600 - Technology 500 - Science |
recordtype |
marc |
publishDateSort |
2016 |
contenttype_str_mv |
zzz |
container_start_page |
18 |
author_browse |
Colpitts, Che C. |
container_volume |
218 |
physical |
7 |
class |
610 610 DE-600 610 VZ 570 540 VZ |
format_se |
Elektronische Aufsätze |
author-letter |
Colpitts, Che C. |
doi_str_mv |
10.1016/j.virusres.2015.09.013 |
dewey-full |
610 570 540 |
title_sort |
high-throughput approaches to unravel hepatitis c virus-host interactions |
title_auth |
High-throughput approaches to unravel hepatitis C virus-host interactions |
abstract |
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. |
abstractGer |
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. |
abstract_unstemmed |
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. |
collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA |
title_short |
High-throughput approaches to unravel hepatitis C virus-host interactions |
url |
https://doi.org/10.1016/j.virusres.2015.09.013 |
remote_bool |
true |
author2 |
El-Saghire, Hussein Pochet, Nathalie Schuster, Catherine Baumert, Thomas F. |
author2Str |
El-Saghire, Hussein Pochet, Nathalie Schuster, Catherine Baumert, Thomas F. |
ppnlink |
ELV012046744 |
mediatype_str_mv |
z |
isOA_txt |
false |
hochschulschrift_bool |
false |
author2_role |
oth oth oth oth |
doi_str |
10.1016/j.virusres.2015.09.013 |
up_date |
2024-07-06T21:49:07.832Z |
_version_ |
1803867964396535808 |
fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV029577306</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625174654.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2016 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.virusres.2015.09.013</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2016005000027.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV029577306</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0168-1702(15)30069-1</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="a">540</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Colpitts, Che C.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">High-throughput approaches to unravel hepatitis C virus-host interactions</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">7</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Systems biology</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HCV pathogenesis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Hepatitis C virus</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Virus-host interactions</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">El-Saghire, Hussein</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pochet, Nathalie</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schuster, Catherine</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Baumert, Thomas F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Shimura, Tsutomu ELSEVIER</subfield><subfield code="t">AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells</subfield><subfield code="d">2014</subfield><subfield code="d">an international journal of molecular and cellular virology</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV012046744</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:218</subfield><subfield code="g">year:2016</subfield><subfield code="g">day:15</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:18-24</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.virusres.2015.09.013</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">218</subfield><subfield code="j">2016</subfield><subfield code="b">15</subfield><subfield code="c">0615</subfield><subfield code="h">18-24</subfield><subfield code="g">7</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
score |
7.4015017 |