Control of hepatitis B virus replication by interferons and Toll-like receptor signaling pathways

World J Gastroenterol. 2014 Sep 7;20(33):11618-29. doi: 10.3748/wjg.v20.i33.11618.

Abstract

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.

Keywords: Hepatitis B virus; Innate immune response; Interferon; Interferon stimulated genes; Toll-like receptor.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antiviral Agents / therapeutic use
  • Drug Resistance, Viral
  • Gene Expression Regulation, Viral
  • Genotype
  • Hepatitis B / drug therapy
  • Hepatitis B / immunology
  • Hepatitis B / metabolism*
  • Hepatitis B / virology
  • Hepatitis B virus / drug effects
  • Hepatitis B virus / genetics
  • Hepatitis B virus / growth & development*
  • Hepatitis B virus / immunology
  • Hepatitis B virus / metabolism
  • Host-Pathogen Interactions
  • Humans
  • Immunity, Innate
  • Interferons / metabolism*
  • Mutation
  • Signal Transduction*
  • Toll-Like Receptors / metabolism*
  • Treatment Outcome
  • Virus Replication* / drug effects

Substances

  • Antiviral Agents
  • Toll-Like Receptors
  • Interferons