中文摘要：

目的研究QSG7701及HepG2细胞支持HBV复制模式的差异及其内在机制。方法质粒PUCl8HBVI．2转染QSG7701与HepG2细胞后定量检测细胞上清液中HBVDNA和HBsAgl采用基因芯片技术比较分析二者基因表达差异并用实时定量PCR验证。结果HepG2细胞在转染后6d内培养上清液可检出HBVDNA及HBsAg，QSG-7701细胞转染后2周内均可检出HBVDNA及HBsAg，且HBVDNA在10d内保持相对稳定的高水平复制（1×10^7～3×10^7拷贝／m1）；基因芯片检测结果示QSG-7701细胞中与HBV生活周期相关的因子如HLF、RXRα、IL-6高表达，而HBxIP、SPIK1为低表达，MMP3不表达。结论QSG7701支持高水平的HBV复制，并可维持cccDNA池的相对稳定，基因差异表达可能为二者支持不同HBV复制模式提供解释。

英文摘要：

Objective To gain some insights into the critical events relating to HBV transcriptional regulation by comparing HBV replicative characteristics in different cell lines. Methods Hepatic cell lines QSG-7701 and HepG2 were transfected with plasmid PUC18-HBV 1.2 by standard calcium phosphate precipitation method, and 1.0 μg pSEAP2-control vector was included in the transfection procedures to serve as an internal control monitoring the transfection efficiency. Hepatitis B surface antigen （HBsAg） in the medium was detected by ELISA method and HBV DNA was quantitated using fluorescent quantitative PCR. The intracellular HBsAg and HBcAg were detected with immunofluorescent staining. The gene expression profiles of QSG-7701 and HepG2 were compared using oligonucleotide microarray; partial differentially expressed genes were verified with quantitative RT-PCR. Results In the medium of the cultured HepG2 cells, HBsAg and HBV DNA could be detected 6 days after the transfection, whereas in QSG-7701 cells, the HBsAg and HBV DNA could be detected for 2 weeks. The HBV DNA in the culture medium of QSG-7701 was about 50 times more than that of the HepG2 cells which were kept in 1 × 10^7 copies/ml-3 × 10^7 copies/ ml for 0-10 days after the transfection. On the 4th day after the transfection, 20%-30% of the QSG-7701 cells were positive with HBsAg and HBcAg immunofluorescent staining. The gene microarray analysis showed that most transcription factors involved with HBV life cycle in QSG-7701 and HepG2 cells had similar levels, whereas some factors involved with HBV transcriptional regulation and core particle disassembly, such as intedeukin-6 （R = 5.1340）, retinoid X receptor, alpha （R = 5.1268）, hepatic leukemia factor （R = 3.2538）, serine protease PRRS23 （R = 2.8356）, hepatitis B virus x interacting protein （R = 0.4939）, serine protease inhibitor Kazal type 1 （R = 0.0740） and matrix metalloproteinase 3 （negative in QSG-7701） were all differentially expressed by HepG2 cells. Conclusion Different t