TY - JOUR
T1 - Hepatitis C virus host cell interactions uncovered
AU - Gottwein, Judith
AU - Bukh, Jens
PY - 2007
Y1 - 2007
N2 - Insights into virus-host cell interactions as uncovered by Randall et al. (1) in a recent issue of PNAS further our understanding of the hepatitis C virus (HCV) life cycle, persistence, and pathogenesis and might lead to the identification of new therapeutic targets. HCV persistently infects 180 million individuals worldwide, causing chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. The only approved treatment, combination therapy with IFN- and ribavirin, targets cellular pathways (2); however, a sustained virologic response is achieved only in approximately half of the patients treated. Therefore, there is a pressing need for the identification of novel drugs against hepatitis C. Although most research focuses on the development of HCV-specific antivirals, such as protease and polymerase inhibitors (3), cellular targets could be pursued and might allow the development of broad-spectrum antivirals (2). Because of the lack of HCV cell culture models, initial studies on HCV-host cell interactions used expressed or purified proteins. The impact of host cell proteins on HCV replication and entry could be studied after the development of the HCV replicon system (reviewed in ref. 1; see also ref. 4) and pseudoviral particles (5), respectively. Both systems were originally developed in the human hepatocellular carcinoma cell line Huh7. Randall et al. (1) investigated for the first time the biological relevance of a panel of putative cellular HCV interacting factors, identified in the described experimental systems and the current study, for the complete viral life cycle using a recently developed HCV genotype 2a (J6/JFH1) cell culture system (6), which uses the Huh7-derived highly permissible cell line Huh7.5 (7). After silencing of individual cellular proteins by using experimental RNA interference
AB - Insights into virus-host cell interactions as uncovered by Randall et al. (1) in a recent issue of PNAS further our understanding of the hepatitis C virus (HCV) life cycle, persistence, and pathogenesis and might lead to the identification of new therapeutic targets. HCV persistently infects 180 million individuals worldwide, causing chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. The only approved treatment, combination therapy with IFN- and ribavirin, targets cellular pathways (2); however, a sustained virologic response is achieved only in approximately half of the patients treated. Therefore, there is a pressing need for the identification of novel drugs against hepatitis C. Although most research focuses on the development of HCV-specific antivirals, such as protease and polymerase inhibitors (3), cellular targets could be pursued and might allow the development of broad-spectrum antivirals (2). Because of the lack of HCV cell culture models, initial studies on HCV-host cell interactions used expressed or purified proteins. The impact of host cell proteins on HCV replication and entry could be studied after the development of the HCV replicon system (reviewed in ref. 1; see also ref. 4) and pseudoviral particles (5), respectively. Both systems were originally developed in the human hepatocellular carcinoma cell line Huh7. Randall et al. (1) investigated for the first time the biological relevance of a panel of putative cellular HCV interacting factors, identified in the described experimental systems and the current study, for the complete viral life cycle using a recently developed HCV genotype 2a (J6/JFH1) cell culture system (6), which uses the Huh7-derived highly permissible cell line Huh7.5 (7). After silencing of individual cellular proteins by using experimental RNA interference
M3 - Journal article
SN - 0027-8424
VL - 104
SP - 13215
EP - 13216
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 33
ER -
