作者
Thomas Kuntzen, Joerg Timm, Andrew Berical, Niall Lennon, Aaron M Berlin, Sarah K Young, Bongshin Lee, David Heckerman, Jonathan Carlson, Laura L Reyor, Marianna Kleyman, Cory M McMahon, Christopher Birch, Julian Schulze zur Wiesch, Timothy Ledlie, Michael Koehrsen, Chinnappa Kodira, Andrew D Roberts, Georg M Lauer, Hugo R Rosen, Florian Bihl, Andreas Cerny, Ulrich Spengler, Zhimin Liu, Arthur Y Kim, Yanming Xing, Arne Schneidewind, Margaret A Madey, Jaquelyn F Fleckenstein, Vicki M Park, James E Galagan, Chad Nusbaum, Bruce D Walker, Gerond V Lake‐Bakaar, Eric S Daar, Ira M Jacobson, Edward D Gomperts, Brian R Edlin, Sharyne M Donfield, Raymond T Chung, Andrew H Talal, Tony Marion, Bruce W Birren, Matthew R Henn, Todd M Allen
发表日期
2008/12
期刊
Hepatology
卷号
48
期号
6
页码范围
1769-1778
出版商
Wiley Subscription Services, Inc., A Wiley Company
简介
Resistance mutations to hepatitis C virus (HCV) nonstructural protein 3 (NS3) protease inhibitors in <1% of the viral quasispecies may still allow >1000‐fold viral load reductions upon treatment, consistent with their reported reduced replicative fitness in vitro. Recently, however, an R155K protease mutation was reported as the dominant quasispecies in a treatment‐naïve individual, raising concerns about possible full drug resistance. To investigate the prevalence of dominant resistance mutations against specifically targeted antiviral therapy for HCV (STAT‐C) in the population, we analyzed HCV genome sequences from 507 treatment‐naïve patients infected with HCV genotype 1 from the United States, Germany, and Switzerland. Phylogenetic sequence analysis and viral load data were used to identify the possible spread of replication‐competent, drug‐resistant viral strains in the population and to infer the …
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