Cellular genomic sites of hepatitis B virus DNA integration

• Verfasst von: Budzinska, Magdalena A. [VerfasserIn]
• Verfasst von: Shackel, Nicholas A. [VerfasserIn]
• Verfasst von: Urban, Stephan [VerfasserIn]
• Verfasst von: Tu, Thomas [VerfasserIn]
• Titel: Cellular genomic sites of hepatitis B virus DNA integration
• Verf.angabe: Magdalena A. Budzinska, Nicholas A. Shackel, Stephan Urban and Thomas Tu
• E-Jahr: 2018
• Jahr: 20 July 2018
• Umfang: 18 S.
• Fussnoten: Gesehen am 24.10.2019
• Titel Quelle: Enthalten in: Genes
• Ort Quelle: Basel : MDPI, 2009
• Jahr Quelle: 2018
• Band/Heft Quelle: 9(2018,7) Artikel-Nummer 365, 18 Seiten
• ISSN Quelle: 2073-4425
• DOI: doi:10.3390/genes9070365
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: cancer evolution
• Sach-SW: chromosomal instability
• Sach-SW: clonal expansion
• Sach-SW: Hepatitis B Virus
• Sach-SW: hepatocellular carcinoma (HCC)
• Sach-SW: insertional mutagenesis
• Sach-SW: inverse nested PCR
• Sach-SW: next generation sequencing
• Sach-SW: non-homologous end joining
• Sach-SW: viral persistence
• K10plus-PPN: 1679753703

Abstract

Infection with the Hepatitis B Virus (HBV) is one of the strongest risk-factors for liver cancer (hepatocellular carcinoma, HCC). One of the reported drivers of HCC is the integration of HBV DNA into the host cell genome, which may induce pro-carcinogenic pathways. These reported pathways include: induction of chromosomal instability; generation of insertional mutagenesis in key cancer-associated genes; transcription of downstream cancer-associated cellular genes; and/or formation of a persistent source of viral protein expression (particularly HBV surface and X proteins). The contribution of each of these specific mechanisms towards carcinogenesis is currently unclear. Here, we review the current knowledge of specific sites of HBV DNA integration into the host genome, which sheds light on these mechanisms. We give an overview of previously-used methods to detect HBV DNA integration and the enrichment of integration events in specific functional and structural cellular genomic sites. Finally, we posit a theoretical model of HBV DNA integration during disease progression and highlight open questions in the field.