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A role for the host DNA damage response in Hepatitis B Virus cccDNA formation-and beyond?
Viruses 9:E125 (2017)
Chronic hepatitis B virus (HBV) infection puts more than 250 million people at a greatly increased risk to develop end-stage liver disease. Like all hepadnaviruses, HBV replicates via protein-primed reverse transcription of a pregenomic (pg) RNA, yielding an unusually structured, viral polymerase-linked relaxed-circular (RC) DNA as genome in infectious particles. Upon infection, RC-DNA is converted into nuclear covalently closed circular (ccc) DNA. Associating with cellular proteins into an episomal minichromosome, cccDNA acts as template for new viral RNAs, ensuring formation of progeny virions. Hence, cccDNA represents the viral persistence reservoir that is not directly targeted by current anti-HBV therapeutics. Eliminating cccDNA will thus be at the heart of a cure for chronic hepatitis B. The low production of HBV cccDNA in most experimental models and the associated problems in reliable cccDNA quantitation have long hampered a deeper understanding of cccDNA molecular biology. Recent advancements including cccDNA-dependent cell culture systems have begun to identify select host DNA repair enzymes that HBV usurps for RC-DNA to cccDNA conversion. While this list is bound to grow, it may represent just one facet of a broader interaction with the cellular DNA damage response (DDR), a network of pathways that sense and repair aberrant DNA structures and in the process profoundly affect the cell cycle, up to inducing cell death if repair fails. Given the divergent interactions between other viruses and the DDR it will be intriguing to see how HBV copes with this multipronged host system.
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Publication type
Article: Journal article
Document type
Review
Keywords
Dna Damage Response ; Dna Repair ; Hbv Cure ; Hbv Minichromosome ; Cccdna ; Hepatitis B Virus; Closed Circular Dna; Nucleotide Excision-repair; Primary Tupaia Hepatocytes; Double-strand Break; X-protein; Core Protein; In-vivo; Hbx Protein; Nonhepatotoxic Degradation; Hepatocellular-carcinoma
ISSN (print) / ISBN
1999-4915
e-ISSN
1999-4915
Journal
Viruses
Quellenangaben
Volume: 9,
Issue: 5,
Article Number: E125
Publisher
MDPI
Publishing Place
Basel
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Virology (VIRO)