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Schreiner, S. ; Nassal, M.*

A role for the host DNA damage response in Hepatitis B Virus cccDNA formation-and beyond?

Viruses 9:E125 (2017)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter 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
Sprache englisch
Veröffentlichungsjahr 2017
HGF-Berichtsjahr 2017
ISSN (print) / ISBN 1999-4915
e-ISSN 1999-4915
Zeitschrift Viruses
Quellenangaben Band: 9, Heft: 5, Seiten: , Artikelnummer: E125 Supplement: ,
Verlag MDPI
Verlagsort Basel
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Virology (VIRO)
POF Topic(s) 30203 - Molecular Targets and Therapies
Forschungsfeld(er) Immune Response and Infection
PSP-Element(e) G-502700-007
PubMed ID 28531167
DOI 10.3390/v9050125
WOS ID WOS:000404226000032
Scopus ID 85019618738
Erfassungsdatum 2017-07-10
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