Hepatitis B virus DNA integration (HBV-DNA integration)

Hepatitis B virus DNA integration refers to the insertion of HBV DNA fragments into the host (human) genome, predominantly in liver cells. This integration occurs at sites of cellular double-stranded DNA breaks, utilizing repair pathways such as non-homologous end joining (NHEJ) or microhomology-mediated end joining (MMEJ). HBV-DNA integration can result in the dysregulation of neighboring host genes, production of chimeric virus-host transcripts, chromosomal instability, and epigenetic changes. Integrated HBV DNA is a source of viral proteins and is implicated in the development and progression of hepatocellular carcinoma. It represents a major barrier to HBV cure because it maintains HBsAg production independently of cccDNA. HBV-DNA integration is not a receptor, enzyme, or molecule directly targeted by drugs, but rather a pathogenic event and a biomarker of advanced HBV-related disease[1][3][4][6][7].

Other names

HBV integrationHBV DNA host integrationintegrated HBV DNA

None (drugs do not act directly on HBV-DNA integration, but indirectly slow HBV replication, thus reducing the number of integration events)