Cheng Z, Zhi X, Sun G, Guo W, Huang Y, Sun W, Tian X, Zhao F, Hu K.
J Med Virol. 2015 Aug 31. doi: 10.1002/jmv.24366. [Epub ahead of print]
Abstract
Hepatitis B virus (HBV) infection is one of the most serious and prevalent health problems worldwide. Current anti-HBV medications have a number of drawbacks, such as adverse effects and drug resistance; thus, novel potential anti-HBV reagents are needed. Selenium (Se) has been shown to be involved in both human immunodeficiency virus and hepatitis C virus infections, but its role in HBV infection remains unclear. To address this, sodium selenite (Na2 SeO3 ) was applied to three HBV cell models: HepG2.2.15 cells, and HuH-7 cells transfected with either 1.1× or 1.3× HBV plasmids. Cytotoxicity of Na2 SeO3 was examined by Cell Counting Kit-8. Levels of viral antigen expression, transcripts, and encapsidated viral DNA were measured by enzyme-linked immunosorbent assay, northern blot, and Southern blot, respectively. There was no obvious cytotoxicity in either HepG2.2.15 or HuH-7 cells with <2.5？μM Na2 SeO3 . Below this concentration, Na2 SeO3 suppressed HBsAg and HBeAg production, HBV transcript level, and amount of genomic DNA in all three tested models, and suppression level was enhanced in line with increases in Na2 SeO3 concentration or treatment time. Moreover, the inhibitory effect of Na2 SeO3 on HBV replication can be further enhanced by combined treatment with lamivudine, entecavir, or adefovir. Thus, the present study clearly proves that Na2 SeO3 suppresses HBV protein expression, transcription and genome replication in hepatoma cell models in a dose- and time-dependent manner. This article is protected by copyright.
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