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Open Access Highly Accessed Review

Innate immune responses in hepatitis B virus (HBV) infection

Aurelia Busca1* and Ashok Kumar2

Author Affiliations

1 Departments of Pathology and Laboratory Medicine, University of Ottawa, 451 Smyth Road, Ottawa, Ontario K1H 8M5, Canada

2 Biochemistry, Microbiology and Immunology, and Infectious Disease & Vaccine Research Centre, Research Institute, Children’s Hospital of Eastern Ontario, University of Ottawa, Ottawa Ontario, Canada

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Virology Journal 2014, 11:22  doi:10.1186/1743-422X-11-22

Published: 7 February 2014

Abstract

Hepatitis B virus (HBV) infection has a low rate of chronicity compared to HCV infection, but chronic liver inflammation can evolve to life threatening complications. Experimental data from HBV infected chimpanzees and HBV transgenic mice have indicated that cytotoxic T cells are the main cell type responsible for inhibition of viral replication, but also for hepatocyte lysis during chronic HBV infection. Their lower activation and impaired function in later stages of infection was suggested as a possible mechanism that allowed for low levels of viral replication. The lack of an interferon response in these models also indicated the importance of adaptive immunity in clearing the infection. Increased knowledge of the signalling pathways and pathogen associated molecular patterns that govern activation of innate immunity in the early stages of viral infections in general has led to a re-evaluation of the innate immune system in HBV infection. Numerous studies have shown that HBV employs active strategies to evade innate immune responses and induce immunosuppression. Some of the immune components targeted by HBV include dendritic cells, natural killer cells, T regulatory cells and signalling pathways of the interferon response. This review will present the current understanding of innate immunity in HBV infection and of the challenges associated with clearing of the HBV infection.

Keywords:
HBV; Innate immunity; Cytokines; Interferon response; TLRs; RIG-I