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Zhang, D.* ; Zhang, K. ; Protzer, U. ; Zeng, C.*

HBV integration induces complex interactions between host and viral genomic functions at the insertion site.

J. Clin. Transl. Hepatol. 9, 399-408 (2021)
Verlagsversion DOI PMC
Free journal
Creative Commons Lizenzvertrag
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. TERT], lysine methyltransferase 2B [i.e. KMT2B], cyclin E1 [CCNE1], and cyclin A2 [CCNA2]). Consequently, distinct genomic features within diverse integrations differentiate their biological functions. Meanwhile, accumulating evidence has shown that viral proteins produced by integrants may cause cell damage even after the suppression of HBV replication. The integration-derived gene products can also serve as tumor markers, promoting the development of novel therapeutic strategies for HCC. Viral integrants can be single copy or multiple copies of different fragments with complicated rearrangement, which warrants elucidation of the whole viral integrant arrangement in future studies. All of these considerations underlie an urgent need to develop novel methodology and technology for sequence characterization and function evaluation of integration events in chronic hepatitis B-associated disease progression by monitoring both host genomic features and viral integrants. This endeavor may also serve as a promising solution for evaluating the risk of tumorigenesis and as a companion diagnostic for designing therapeutic strategies targeting integration-related disease complications.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Korrespondenzautor
Schlagwörter Chimeric Reads ; Double-strand Break ; Fusion Transcript ; Junction Reads ; Virus Cell Junction ; Virus Cellular Junction ; Virus Host Junction; Hepatitis-b-virus; Double-strand Breaks; Hepatocellular-carcinoma; Dna Integration; X-protein; Mevalonate Kinase; Human Hepatocytes; Clonal Expansion; Cellular-dna; Liver
ISSN (print) / ISBN 2225-0719
e-ISSN 2310-8819
Zeitschrift Journal of Clinical and Translational Hepatology
Quellenangaben Band: 9, Heft: 3, Seiten: 399-408 Artikelnummer: , Supplement: ,
Verlag Xia & He Publishing Limited
Verlagsort Second Affiliated Hosp Chongqing Medical Univ, 14090 Southwest Freeway, Ste 300, Sugar Land, Tx 77478 Usa
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Virology (VIRO)
Förderungen National Natural Science Foundation of China
Innovation Promotion Association CAS
111Project