Hepatitis C viral kinetics in special populations

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Abstract
Mathematical models of hepatitis C viral kinetics provide a means of estimating the antiviral effectiveness of therapy, the rate of virion clearance, and the rate of loss of hepatitis C virus (HCV)-infected cells. They have also proved useful in evaluating the extrahepatic contribution to HCV plasma viremia and have suggested mechanisms of action for interferon-α and ribavirin. Viral kinetic models can explain the observed HCV RNA profiles under treatment—for example, flat partial response, biphasic and triphasic viral decay, and viral rebound. Current therapy with (pegylated) interferon-α and ribavirin has poorer success in patients with insulin resistance, hepatic fibrosis, African American ethnicity, HCV/HIV-coinfection, HCV genotype 1, or high baseline viral load. Mathematical modeling and statistical analysis of experimental data have been useful in understanding some of these treatment obstacles.