HBV Integration Induces Complex Interactions between Host and Viral Genomic Functions at the Insertion Site.
Chimeric reads
Double-strand break
Fusion transcript
Junction reads
Virus cell junction
Virus cellular junction
Virus host junction
Journal
Journal of clinical and translational hepatology
ISSN: 2225-0719
Titre abrégé: J Clin Transl Hepatol
Pays: United States
ID NLM: 101649815
Informations de publication
Date de publication:
28 Jun 2021
28 Jun 2021
Historique:
received:
07
02
2021
revised:
29
03
2021
accepted:
31
03
2021
entrez:
5
7
2021
pubmed:
6
7
2021
medline:
6
7
2021
Statut:
ppublish
Résumé
Hepatitis B virus (HBV), one of the well-known DNA oncogenic viruses, is the leading cause of hepatocellular carcinoma (HCC). In infected hepatocytes, HBV DNA can be integrated into the host genome through an insertional mutagenesis process inducing tumorigenesis. Dissection of the genomic features surrounding integration sites will deepen our understanding of mechanisms underlying integration. Moreover, the quantity and biological activity of integration sites may reflect the DNA damage within affected cells or the potential survival benefits they may confer. The well-known human genomic features include repeat elements, particular regions (such as telomeres), and frequently interrupted genes (e.g., telomerase reverse transcriptase [i.e.
Identifiants
pubmed: 34221926
doi: 10.14218/JCTH.2021.00062
pii: JCTH.2021.00062
pmc: PMC8237140
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
399-408Informations de copyright
© 2021 Authors.
Déclaration de conflit d'intérêts
Dake Zhang has an authorized patent for the probe-based HBV DNA capture in plasma as a liquid biopsy to monitor HCC development. The other authors have no conflict of interests related to this publication.
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