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Review
. 2015 Jun;26(1-2):1-8.
doi: 10.1007/s13337-015-0247-y. Epub 2015 Apr 5.

Hepatitis B virus infection: An insight into infection outcomes and recent treatment options

Affiliations
Review

Hepatitis B virus infection: An insight into infection outcomes and recent treatment options

Faseeha Noordeen. Virusdisease. 2015 Jun.

Abstract

Hepatitis B virus (HBV) currently infects an estimated population of 2 billion individuals in the world, including 400 million people with chronic HBV infection. HBV virology, replication and the host's immune response to HBV infection contribute to different infection outcomes. Acute hepatitis HBV infection is self-limiting but it leaves a residual infection that can become active in an individual during immunosuppression. In chronic HBV infection, the virus persistently replicates in hepatocytes leading to immune mediated hepatocellular damage. Despite the inability to remove the virus in more than 70 % of patients, current treatments for chronic HBV infection, interferon alpha and antiviral nucleotide/nucleoside analogues, aim to reduce viral replication to prevent or at least delay the progression to cirrhosis and hepatocellular carcinoma. In both self resolved acute and persistent HBV infection, the long term existence of chromatinised covalently closed circular DNA (cccDNA) in the nuclei of infected hepatocytes cannot be targeted by current treatments to eliminate these templates to eradicate the viral persistence. Identifying the mechanisms involve in the removal of infected hepatocytes will be useful as treatment options. In this context, DNA based novel therapeutic and immunization strategies might help to remove stable cccDNA and thus viral persistence.

Keywords: Hepatitis B virus; Infection outcomes; Natural history; Vaccination and treatment.

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Figures

Fig. 1
Fig. 1
Schematic diagram showing the different stages of hepadnavirus life cycle during replication—adapted from Jilbert et al. [17]. cccDNA Covalently closed circular DNA, RT Reverse transcriptase, rcDNA Relaxed circular DNA, DSL DNA Double stranded linear DNA
Fig. 2
Fig. 2
Natural history illustrating the different phases of chronic HBV infection—adapted from Yuen and Lai [39]. HBeAg HBV e antigen, HBsAg HBV surface antigen, HCC hepatocellular carcinoma, ALT alanine aminotransferase

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