Fig. 3. HCV attenuation of IFN signaling.

Fig. 3

HCV attenuation of IFN signaling. IFN α/β Receptor signaling by IFN from autocrine/paracrine and therapeutic sources is subject to feedback inhibition by suppressor of cytokine signaling (SOCS) proteins. The HCV core protein can induce the expression of SOCS-3, which suppresses Jak-STAT signaling events (Alexander, 2002). Expression of the protein inhibitor of activated STAT (PIAS) is induced by HCV proteins, possibly mediated by protein phosphatase 2A (PP2A) signaling events and STAT demethylation (Duong et al., 2004). This blocks STAT1 function. Some patients with chronic HCV infection exhibit aberrantly high levels of serum IL-8 (Polyak et al., 2001b). The biological activity of IL-8 interferes with IFN signaling events (Khabar et al., 1997). HCV modulation of IFN signaling allows the virus to evade the antiviral actions of the host response and IFN therapy.

From: Chapter 13, HCV Regulation of Host Defense

Cover of Hepatitis C Viruses
Hepatitis C Viruses: Genomes and Molecular Biology.
Tan SL, editor.
Norfolk (UK): Horizon Bioscience; 2006.
Copyright © 2006, Horizon Bioscience.

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