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Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle
Published on: February 1, 2017
Cellular cIAP2 gene expression associated with anti-HBV activity of TNF-alpha in hepatoblastoma cells
Xiaoying Liu1, Junjie Shao, Wei Xiong
1Key Laboratory of Medical Molecular Virology, Shanghai Medical College, and Institute of Biomedical Science and Microbiology, Fudan University, Shanghai 200032, China.
Abstract:
Hepatitis B virus (HBV)-specific cytotoxic T lymphocytes (CTLs) can abolish HBV gene expression and replication through a noncytopathic mechanism mediated by tumor necrosis factor-alpha (TNF-alpha). However, the molecular mechanisms of TNF-alpha antiviral activity are not completely understood. To examine TNF-alpha-induced cellular responses and identify genes involved in anti-HBV activity, cDNA microarrays dotted with 14, 112 human genes were used to examine the transcriptional changes in HepG2 after treatment with TNF-alpha for 6 h. The results showed that many genes related to ligands and receptors, signal transduction including the TNF-alpha signaling pathway, mitochondrial and ribosomal proteins, and transcription regulation were induced by TNF-alpha. Interestingly, the TNF-alpha-inducible gene cIAP2 was found to inhibit HBV protein synthesis, viral replication, and transcription. Taken together, our results revealed the global effects of TNF-alpha treatment on hepatocellular gene expression. The antiviral genes identified by microarray could be developed as potential new anti-HBV drugs or for other novel therapies.
