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Review
.2014 Oct 7;20(37):13293-305.
doi: 10.3748/wjg.v20.i37.13293.

Update on hepatitis B virus infection

Affiliations
Review

Update on hepatitis B virus infection

Chan Ran You et al. World J Gastroenterol..

Abstract

Chronic infection with hepatitis B virus (HBV) leads to the development of hepatocellular carcinoma and/or chronic liver failure. Despite extensive research, the immunopathogenesis is not completely understood. Viral persistence and clinical outcomes following HBV infection depend on viral factors and host factors; including genetic factors that determine a host's immune mechanisms. The primary goal of chronic hepatitis B (CHB) treatment is to eradicate HBV or to at least maintain suppression of HBV replication. Despite recent advances in anti-viral agents for chronic HBV infection, complete eradication of the virus has been difficult to achieve. Agents for the treatment of CHB are divided mainly into two groups: immunomodulating agents and antiviral nucleos(t)ide analogues (NAs). Although NAs are safe, effective and easily administered orally, their long-term use poses the risk of drug resistance. Currently, international evidence-based guidelines have been developed to support physicians in managing CHB patients. However, treatment of patients with drug resistance is still challenging, as only a few classes of anti-HBV drugs are available and cross-resistance between drugs can occur. In addition, as the currently available genotypic test for detection of drug resistance still has limitations in identifying the different substitutions present in the same viral genome, the development of a new virologic test to overcome this limitation is necessary. Among the predictive factors associated with response to pegylated interferon (PEG-IFN) therapy, hepatitis B surface antigen quantification is considered to be a surrogate marker for monitoring response to PEG-IFN. Current practice guidelines stress the importance of profound and durable HBV viral suppression in the treatment of CHB patients. To this end, it is essential to choose a potent antiviral drug with a low risk of resistance for initial treatment of CHB to achieve sustained virological response. This review highlights recent advances in the understanding of the immunopathogenesis of HBV and currently available and developing treatment strategies against HBV infection.

Keywords: Antiviral therapy; Chronic hepatitis B; Hepatitis B virus; Nucleos(t)ide analogue; Pegylated interferon.

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Figures

Figure 1
Figure 1
Summary of the innate immune response and cellular immune response against hepatitis B virus. Natural killer (NK) cells, natural killer T (NKT) cells, dendritic cells, cytokines, chemokines and toll-like receptor (TLR) contribute to the innate immune response against hepatitis B virus (HBV). Also, NK cells, NKT and macrophages can inhibit HBV replication by producing interleukin (IL)-12 and nitric oxide. Dysfunction of the innate immune response in the immune tolerant phase may be explained by this process. However, HBeAg reduces TLR2 expression on hepatocytes, Kupffer cells and peripheral monocytes. Moreover, NK cell activation induces TRAIL-mediated death of hepatocytes in CHB, leading to liver injury. Chronic HBV carriers mount a defective T-cell response. CD8+ T cells cause the lysis of HBV-infected hepatocytes through cytolytic and non-cytolytic mechanisms. Non-cytolytic mechanisms are mediated by some specific cytokines, such as interferon (IFN)-γ and tumor necrosis factor (TNF)-α which selectively degrade replicating genomes of HBV without killing infected cells. In CHB, Tregs suppress effector T cells, which impair the cellular immune response. The programmed death-1 (PD-1) inhibitory receptor is involved in the impairment of virus-specific CD8 T-cell function.
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References

    1. Rehermann B, Nascimbeni M. Immunology of hepatitis B virus and hepatitis C virus infection. Nat Rev Immunol. 2005;5:215–229. - PubMed
    1. Liang TJ. Hepatitis B: the virus and disease. Hepatology. 2009;49:S13–S21. - PMC - PubMed
    1. Ganem D, Prince AM. Hepatitis B virus infection--natural history and clinical consequences. N Engl J Med. 2004;350:1118–1129. - PubMed
    1. Iloeje UH, Yang HI, Su J, Jen CL, You SL, Chen CJ, Risk Evaluation of Viral Load E, Associated Liver Disease/Cancer-In HBVSG. Predicting cirrhosis risk based on the level of circulating hepatitis B viral load. Gastroenterology. 2006;130:678–686. - PubMed
    1. Chen CJ, Yang HI, Su J, Jen CL, You SL, Lu SN, Huang GT, Iloeje UH, Group R-HS. Risk of hepatocellular carcinoma across a biological gradient of serum hepatitis B virus DNA level. JAMA. 2006;295:65–73. - PubMed

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