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Integration of HBV‐DNA into liver and hepatocellular carcinoma cells during persistent HBV infection
Author(s) -
Shafritz David A.
Publication year - 1982
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240200310
Subject(s) - hepatocellular carcinoma , hbsag , hepatitis b virus , virology , liver disease , dna , virus , biology , hepatitis b , medicine , immunology , cancer research , genetics
The hepatitis B virus carrier state (persistent HBV infection) is characterized by the presence of viral surface antigen (HBsAg) and virion particles (Dane particles) in the blood. From 1% to 10% of carriers develop chronic liver disease and/or hepatocellular carcinoma. Recent studies have demonstrated integrated HBV‐DNA in hepatocellular carcinomas and in several human hepatoma cell lines. In hepatoma patients, integrated HBV‐DNA has been found in all HBsAg carriers. Nontumorous liver also revealed integrated HBV‐DNA with the same or a different hybridization pattern from that observed in the tumor. To explore when integration occurs, carriers of short‐term (<2 years) or long‐term (> 8‐10 years) were evaluated. DNA extracts from percutaneous (needle) liver biopsies showed free viral DNA with no specific integration bands in short‐term carriers. In long‐term carriers, HBV‐DNA was integrated into the host genome with either a diffuse or a unique hybridization pattern. HBV‐DNA integration correlated with the duration of the carrier state and absence of virions in the serum but did not correlate with histologic evidence of chronic hepatitis. These studies suggest that integration of HBV‐DNA occurs during persistent HBV infection irrespective of liver disease and precedes development of hepatocellular carcinoma.