Hepatitis C viral kinetics in the era of direct acting antiviral agents and interleukin-28B

被引：51
作者：
Dahari H. [1 ,2 ]
Guedj J. [2 ]
Perelson A.S. [2 ]
Layden T.J. [1 ]
机构：
[1] Department of Medicine, Section of Hepatology, University of Illinois at Chicago, Chicago, IL 60612
[2] Theoretical Biology and Biophysics, MS-K710, Los Alamos National Laboratory, Los Alamos
来源：
Current Hepatitis Reports | 2011年 / 10卷 / 3期
基金：
美国国家卫生研究院;
关键词：
Direct acting antiviral agents; Hepatitis C virus; IL28B polymorphism; Interleukin; 28B; Mathematical modeling; Pegylated interferon-α; Ribavirin; Viral kinetics;
D O I：
10.1007/s11901-011-0101-7
中图分类号：
学科分类号：
摘要：
In the last decade, hepatitis C virus (HCV) kinetics has become an important clinical tool for the optimization of therapy with pegylated-interferon-α (PEG-IFN) and ribavirin (RBV). Mathematical models have generated important insights into HCV pathogenesis, HCV-host dynamics, as well as IFN and RBV modes of action. Clinical trials with directacting antiviral agents (DAAs) against various steps of the HCV-life cycle have revealed new viral-kinetic patterns that have not been observed with (PEG)-IFN+RBV. Very recently, studies have shown that single nucleotide polymorphisms (SNPs) in the interleukin-28B (IL28B) gene region were associated with race/ethnicity, and with response to PEG-IFN +RBV. Here, we review our current knowledge of HCV kinetics and related mathematical models during (PEG)-IFN +RBVand/or DAA-based therapies, HCV pathogenesis, and the role of IL28B polymorphism on early HCV kinetics. Better understanding of the mode of actions of drugs and viral kinetics may help to develop new, individualized therapeutic regimens that include DAAs in combination with PEG-IFN+RBV. © Springer Science+Business Media, LLC (outside the USA) 2011.
引用
收藏
页码：214 / 227
页数：13
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