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

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 a...

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Bibliographic Details
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
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Summary: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.
ISSN:1999-4915
1999-4915
DOI:10.3390/v16040609