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A Three-Dimensional Spheroid Model to Investigate the Tumor-Stromal Interaction in Hepatocellular Carcinoma
Published on: September 30, 2021
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Hepatitis D Virus and Hepatocellular Carcinoma
Patrizia Farci1, Grazia Anna Niro2, Fausto Zamboni3
1Hepatic Pathogenesis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Viruses
|June 2, 2021
Summary
Hepatitis D virus (HDV), dependent on Hepatitis B virus (HBV), significantly increases hepatocellular carcinoma (HCC) risk. HDV-associated liver cancer shows unique molecular changes, suggesting distinct oncogenic mechanisms.
Area of Science:
- Hepatology
- Virology
- Oncology
Background:
- Hepatitis D virus (HDV) is a defective RNA virus requiring Hepatitis B virus (HBV) for replication and transmission.
- Chronic Hepatitis D is a severe liver disease associated with high rates of cirrhosis, liver decompensation, and hepatocellular carcinoma (HCC).
- The oncogenic role of HDV and its specific contribution to hepatocarcinogenesis remain under investigation.
Purpose of the Study:
- To investigate the molecular mechanisms by which HDV contributes to the development of HCC.
- To compare the molecular profile of HCC in HDV-HBV coinfection versus HBV monoinfection.
Main Methods:
- Analysis of molecular profiles of hepatocellular carcinoma (HCC) in patients with HDV-HBV coinfection.
- Comparison of gene expression patterns between HDV-HCC and HBV-HCC.
Main Results:
- Hepatocellular carcinoma (HCC) in HDV-HBV coinfection exhibits a unique molecular signature distinct from HBV monoinfection-associated HCC.
- Upregulated genes in HDV-HCC are enriched in pathways related to cell-cycle/DNA replication and DNA damage/repair.
- These findings suggest genome instability as a key mechanism in HDV-driven hepatocarcinogenesis.
Conclusions:
- HDV infection is associated with a distinct molecular profile in HCC, implicating genome instability in its oncogenesis.
- Despite dependence on HBV, HDV and HBV appear to promote carcinogenesis through different molecular pathways.
- Further research is needed to elucidate the precise mechanisms of HDV-induced liver cancer.
Keywords:
HBV replicationHDV replicationHepatitis D viruscirrhosishepatocellular carcinomatranscriptomics
