Here we review our current knowledge of HCV kinetics under IFN-based therapy and newly developed antiviral agents specifically targeted to attack HCV, and show how mathematical models have helped improve our understanding of HCV infection and treatment.

The current recommended therapy for chronic hepatitis C is the combination of peginterferon and ribavirin, which results in a sustained clearance of hepatitis C virus (HCV) in at least half of patients. However, the mechanisms by which interferon alpha (IFN- α) and ribavirin act against HCV are not well defined.

Jun 7, 2013 · For the past 25 years, recombinant interferon-α (IFNα) has been the main component of treatments for HCV infection. Treatment efficacy has shown a stepwise improvement following the...

As interferon targets the HCV virus by activating the immune system, which has a broad spectrum of activities, IFN treatment comes with many side effects which lead to poor patient compliance to antiviral therapy.

Interferon (IFN)-α, a type-I IFN, is widely used to treat chronic hepatitis C virus (HCV) infection, but the broad expression of IFN-α receptors often leads to adverse reactions in many organs. Here, we examine IFN-λ, a type-III IFN, as a therapeutic alternative to IFN-α.

Aug 5, 2010 · Chronic infection with hepatitis C virus (HCV) is associated with significant liver disease and is therefore an important public health problem. The current standard-of-care therapy for chronic HCV infection consists of a combination of pegylated (PEG) interferon (IFN)-α …

Apr 8, 2020 · Hepatocytes infected with HCV produce types I and III IFNs. These endogenous IFNs upregulate a set of ISGs that negatively impact the outcome of pegylated IFN-α and ribavirin treatments, which were previously used to treat HCV.

Aug 17, 2005 · Interferon-α (IFN-α) was first shown to have beneficial effects in patients with chronic hepatitis C in 1986, well before the identification of the hepatitis C virus (HCV) 1. Once HCV was...

HCV evades the host response through a complex combination of virus-host interactions that disrupt intracellular signaling pathways and attenuate the antiviral actions of IFN. Regulation of the host response breaks a link between innate and adaptive immunity and provides a foundation for HCV replication and spread.

This review focuses on recent studies on how the ISGs response and the IFNλ genetic factors (interleukin-28B and IFNL4) affect the clinical outcome of HCV infection highlighting their impact in the current antiviral therapies with direct acting antiviral agents.