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Updated: Aug 4, 2026
09:02
Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
Published on: June 5, 2020
[Hepatitis B virus and hepatocellular carcinoma]
P Tiollais1, A Dejean, M A Buendia
1INSERM U. 163, Institut Pasteur, Paris.
Bulletin De L'Academie Nationale De Medecine
|February 1, 1991
Summary
Woodchuck hepatitis virus integration near the c-myc oncogene contributes to liver tumor development. Hepatitis B virus (HBV) insertion in humans may also cause liver cancer through insertional mutagenesis.
Area of Science:
- Hepatology and Viral Oncology
- Molecular Biology and Genetics
Background:
- Hepatocellular carcinoma (HCC) development is complex, with viral involvement suspected.
- Proto-oncogene activation by viral integration is a potential mechanism in carcinogenesis.
Purpose of the Study:
- To investigate the role of woodchuck hepatitis virus (WHV) integration near the c-myc oncogene in woodchuck liver tumors.
- To explore the mechanism of hepatitis B virus (HBV) insertional mutagenesis in human hepatoma.
Main Methods:
- Characterization of WHV integration sites in woodchuck HCC.
- Comparative analysis of HBV integration site in human hepatoma with unoccupied sites.
- Isolation and characterization of the affected gene (hap).
Main Results:
- WHV integration near c-myc in woodchuck tumors led to overexpression of c-myc transcripts.
- HBV DNA insertion in a human hepatoma occurred within a putative exon similar to thyroid/steroid hormone receptors.
- The hap gene, encoding the retinoic acid receptor, was identified and shown to be altered by HBV insertion.
Conclusions:
- WHV integration near proto-oncogenes can initiate liver tumor formation.
- HBV insertion can lead to the expression of a chimeric retinoic acid receptor, contributing to hepatocellular carcinoma.
- These findings strongly support a direct role for HBV in liver carcinogenesis via insertional mutagenesis.
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