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Published online ahead of print on 4 March 2009 as doi:10.1099/vir.0.007211-0
Journal of General Virology 2009;90:1124.

A more recent version of this article appeared on May 1, 2009 J Gen Virol (2009), DOI 10.1099/vir.0.007211-0
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Hepatitis delta virus epigenetically enhances clusterin expression via histone acetylation in human hepatocellular carcinoma cells

Fu-Tien Liao1, Yi-Ju Lee2, Jiunn-Liang Ko1, Chu-Cheng Tsai1, Chao-Jung Tseng1 and Gwo-Tarng Sheu1,3

1 Institute of Medical and Molecular Toxicology, Chung Shan Medical University;
2 Institute of Immunology, Chung Shan Medical University

3 E-mail: gtsheu{at}csmu.edu.tw

Both isoforms of hepatitis delta antigens (HDAgs) are highly associated with viral proliferation and may act as co-activators of cellular gene expression. Human hepatocellular carcinoma (HCC) cell line Huh7 which stably expresses HDAgs was differentially screened, and the results showed that clusterin gene expression is enhanced. The mechanisms for HDAgs-mediated clusterin gene upregulation were investigated. Expression of HDAgs was associated with enhanced histone H3 acetylation within clusterin promoter on chromatin immunoprecipitation (ChIP) assay. Transient transfection of the HDAg-expressing plasmids into Huh7 cells also enhanced clusterin expression and histone acetylation. Furthermore, hepatitis delta virus (HDV) replication was associated with histone hyperacetylation and clusterin induction. The effect of increased clusterin expression was determined by a chemosensitivity assay with adriamycin (ADR) treatment. Our data indicated that HDV-induced clusterin protein increases cell survival potential. Thus, it is possible that epigenetic regulation by HDV contributes to a pathological outcome of hepatitis D/hepatitis B viral hepatitis and HCC.

Received 11 September 2008; accepted 12 January 2009.




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