Hepatitis B virus biology and life cycle

Senko Tsukuda; Koichi Watashi

doi:10.1016/j.antiviral.2020.104925

Hepatitis B virus biology and life cycle

Antiviral Res. 2020 Oct:182:104925. doi: 10.1016/j.antiviral.2020.104925. Epub 2020 Aug 28.

Authors

Senko Tsukuda¹, Koichi Watashi²

Affiliations

¹ Department of Virology II, National Institute of Infectious Diseases, Tokyo, Japan; Nuffield Department of Medicine, University of Oxford, Oxford, UK.
² Department of Virology II, National Institute of Infectious Diseases, Tokyo, Japan; Department of Applied Biological Science, Tokyo University of Science, Noda, Japan; Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan; MIRAI, JST, Saitama, Japan. Electronic address: kwatashi@nih.go.jp.

PMID: 32866519
DOI: 10.1016/j.antiviral.2020.104925

Abstract

Hepatitis B virus (HBV) specifically infects hepatocytes and causes severe liver diseases. The HBV life cycle is unique in that the genomic DNA (relaxed-circular partially double-stranded DNA: rcDNA) is converted to a molecular template DNA (covalently closed circular DNA: cccDNA) to amplify a viral RNA intermediate, which is then reverse-transcribed back to viral DNA. The highly stable characteristics of cccDNA result in chronic infection and a poor rate of cure. This complex life cycle of HBV offers a variety of targets to develop antiviral agents. We provide here an update on the current knowledge of HBV biology and its life cycle, which may help to identify new antiviral targets.

Keywords: Entry; HBV; Life cycle; NTCP; Replication; cccDNA.

Publication types

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

MeSH terms

Antiviral Agents / therapeutic use
DNA, Viral / genetics
Hep G2 Cells
Hepatitis B / drug therapy
Hepatitis B / virology
Hepatitis B virus / genetics
Hepatitis B virus / growth & development*
Hepatitis B virus / pathogenicity
Hepatocytes / virology*
Host Microbial Interactions
Humans
Virus Replication*

Substances

Antiviral Agents
DNA, Viral