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

• Published in: Viruses 2024-04, Vol.16 (4), p.609
• Main Authors: Gómez-Moreno, Andoni, Ploss, Alexander
• Format: Article
• Language: English
• Subjects: Analysis; Antigens; cccDNA; chemical bonding; chronic hepatitis B; Circular DNA; Cirrhosis; Cytoplasm; DNA polymerase; DNA repair; DNA Replication; DNA viruses; DNA, Circular - genetics; DNA, Viral - genetics; dsDNA viruses; etiological agents; family; Fibrosis; Gene Expression Regulation, Viral; Genetic aspects; Genetic transcription; genome; Genome, Viral; Genomes; Genomics; HBV; Heparan sulfate; Hepatitis B; Hepatitis B - virology; Hepatitis B virus; Hepatitis B virus - genetics; Hepatitis B virus - physiology; Hepatitis B, Chronic - virology; Hepatocellular carcinoma; hepatoma; Humans; Infections; Liver cancer; Methods; Polymerization; Proteins; Review; risk; RNA polymerase; Transcription; transcription (genetics); Transcription factors; Transcription, Genetic; viral hepatitis; viral transcription; Viral Transcription - genetics; Virus Replication; Viruses
• ISSN: 1999-4915; 1999-4915
• DOI: 10.3390/v16040609

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 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.