Mechanisms of Hepatitis B Virus cccDNA and Minichromosome Formation and HBV Gene Transcription

Andoni Gómez-Moreno, Alexander Ploss

Research output: Contribution to journalReview articlepeer-review

Abstract

Hepatitis B virus (HBV) is the etiologic agent of chronic hepatitis B, which puts at least 300 million patients at risk of developing fibrosis, cirrhosis, and hepatocellular carcinoma. HBV is a partially double-stranded DNA virus of the Hepadnaviridae family. While HBV was discovered more than 50 years ago, many aspects of its replicative cycle remain incompletely understood. Central to HBV persistence is the formation of covalently closed circular DNA (cccDNA) from the incoming relaxed circular DNA (rcDNA) genome. cccDNA persists as a chromatinized minichromosome and is the major template for HBV gene transcription. Here, we review how cccDNA and the viral minichromosome are formed and how viral gene transcription is regulated and highlight open questions in this area of research.

Original languageEnglish (US)
Article number609
JournalViruses
Volume16
Issue number4
DOIs
StatePublished - Apr 2024

All Science Journal Classification (ASJC) codes

  • Infectious Diseases
  • Virology

Keywords

  • cccDNA
  • DNA repair
  • HBV
  • hepatitis B virus
  • viral hepatitis
  • viral transcription

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