Interferon-alfa, interferon-lambda and hepatitis C

Abstract

Three new studies report genetic variants near IL28B, which encodes interferon-λ3 (interleukin 28B), are associated with response to treatment of chronic hepatitis C virus infection with interferon-alfa/ribavirin combination therapy. This renews interest in how interferons suppress viremia and could lead to improved clinical decisions for chronic HCv infection treatment based on individual genotype.

Figure 1

The interferon-λ proteins induce the JAK-STAT antiviral pathway by binding to different receptors than interferon-α and interferon-alfa. Genetic association^– and in vitro^, studies suggest that an interactive and complementary relationship between interferon-λ and interferon-α/-alfa may be important for suppressing HCV. IFN, interferon; IRF, interferon-regulatory factor; ISGF, interferon-stimulated gene factor; ISRE, interferon-stimulated response element; JAK, Janus kinase; R, receptor; STAT, signal transducer and activator of transcription; TYK, tyrosine kinase.