Published online Sep 7, 2014. doi: 10.3748/wjg.v20.i33.11618
Revised: February 28, 2014
Accepted: April 15, 2014
Published online: September 7, 2014
Hepatitis B virus (HBV) infection is one of the major causes of liver diseases, affecting more than 350 million people worldwide. The interferon (IFN)-mediated innate immune responses could restrict HBV replication at the different steps of viral life cycle. Indeed, IFN-α has been successfully used for treatment of patients with chronic hepatitis B. However, the role of the innate immune response in HBV replication and the mechanism of the anti-HBV effect of IFN-α are not completely explored. In this review, we summarized the currently available knowledge about the IFN-mediated anti-HBV effect in the HBV life cycle and the possible effectors downstream the IFN signaling pathway. The antiviral effect of Toll-like receptors (TLRs) in HBV replication is briefly discussed. The strategies exploited by HBV to evade the IFN- and TLR-mediated antiviral actions are summarized.
Core tip: Hepatitis B virus (HBV) infection is one of the major causes of liver diseases affecting more than 350 million people worldwide. Interferon (IFN)- and Toll-like receptors (TLR)-mediated innate immune responses could restrict HBV replication at the different steps of viral life cycle. Though a great number of publications in this field appeared during the last years, there is no review to discuss the progress. Here, we summarized the currently available knowledge about the anti-HBV effect of IFNs and TLRs and the possible effectors downstream the IFN signaling pathway. This review provides an overview for scientists working on HBV and related fields.