Dahari Harel, Layden-Almer Jennifer E, Perelson Alan S, Layden Thomas J
Department of Medicine, Section of Hepatology, The University of Illinois at Chicago 840 S. Wood Street MC787, Chicago, IL 60612.
Curr Hepat Rep. 2008;7(3):97-105. doi: 10.1007/s11901-008-0022-2.
Mathematical models of hepatitis C viral (HCV) kinetics provide a means of estimating the antiviral effectiveness of therapy, the rate of virion clearance and the rate of loss of HCV-infected cells. They have also proved useful in evaluating the extrahepatic contribution to HCV plasma viremia and they have suggested mechanisms of action for both interferon-α and ribavirin. Viral kinetic models can explain the observed HCV RNA profiles under treatment, e.g., flat partial response, biphasic and triphasic viral decay and viral rebound. Current therapy with (pegylated) interferon-α and ribavirin has a poorer success in patients having insulin resistance, hepatic fibrosis, African American ethnicity, HCV/HIV-coinfection, HCV genotype-1 and high baseline viral load. The use of mathematical modeling and statistical analysis of experimental data have been useful in understanding some of these treatment obstacles.
丙型肝炎病毒（HCV）动力学的数学模型提供了一种估算治疗的抗病毒效果、病毒粒子清除率以及HCV感染细胞损失率的方法。它们在评估肝外因素对HCV血浆病毒血症的作用方面也已证明是有用的，并且还提示了α干扰素和利巴韦林的作用机制。病毒动力学模型可以解释治疗过程中观察到的HCV RNA谱，例如平缓的部分反应、双相和三相病毒衰减以及病毒反弹。目前使用（聚乙二醇化）α干扰素和利巴韦林进行的治疗，在患有胰岛素抵抗、肝纤维化、非裔美国人种族、HCV/HIV合并感染、HCV基因1型以及高基线病毒载量的患者中成功率较低。运用数学建模和对实验数据进行统计分析，有助于理解其中一些治疗障碍。
