To clarify the role of APOBEC3G (A3G) in cellular defense against hepatitis B virus ( HBV), the expression of A3G in normal human liver and the regulation of the A3G expression in hep-atoma cell line (HuH-7) were investigated. Expression level of APOBEC3s mRNA in human liver was determined by RT-PCR. HuH-7 and HepG2 cells were treated with various concentrations of IFN-α(0 U/ml, 100 U/ml, 500 U/ml, 1000 U/ml)for 12 h. The mRNA levels were measured by a quantitative RT-PCR, the results were normalized relative to the specimens without IFN-αstimulation. Total protein of HuH-7 cells treated with various concentrations of IFN-αfor 48 h was subjected to Western blot analysis. For reporter gene assay, HuH-7 cells were transfected with the reporter plasmids containing IRF-E sites and its mutants with different lengths. Then the cells were treated with or without 1200 U/ml IFN-a for additional 12 h (1000 U/ml) after 24 h of transfection, and the cell lysate was prepared and assayed for luciferase activity. It was found that normal human liver expressed the mRNA of A3G. A3G mRNA expression in HuH-7 and HepG2 cells were up-regulated by IFN-αstimulation in a dose-depen-dent manner. Western blot analysis indicated that A3G protein expression was also enhanced by IFN-αstimulation. Sequence analysis showed the existence of putative sites of IFN regulatory factor element (IRF-E) in 5’ region of A3G gene upstream the initiation codon. IFN-αstimulation results in 6- to 8-fold increase in luciferase activity in cells transfected with the plasmid containing IRF-E sites of the 5’ upstream sequences, whereas luciferase activity did not change in cells transfected with the plasmid containing mutant IRF-E sites or without IRF-E sites. As a conclusion, A3G are expressed in normal human liver. A3G expression was up-regulated by IFN-αstimulation in hepatoma cells and could be involved in host defense mechanisms against HBV. ERF-E site in 5’ region of AP0BEC3G gene upstream the initiation codon plays an important role in this process. To clarify the role of APOBEC3G (A3G) in cellular defense against hepatitis B virus (HBV), the expression of A3G in normal human liver and the regulation of the A3G expression in hep-atoma cell line (HuH-7) were investigated. Expression level of APOBEC3s mRNA in human liver was determined by RT-PCR. HuH-7 and HepG2 cells were treated with various concentrations of IFN-α (0 U / ml, 100 U / ml, 500 U / ml, 1000 U / ml) for 12 h. The mRNA levels were measured by a quantitative RT-PCR, the results were normalized relative to the specimens without IFN-αstimulation. Total protein of HuH-7 cells treated with various concentrations of IFN-αfor 48 h was subjected to Western blot analysis. For reporter gene assay, HuH-7 cells were transfected with the reporter plasmids containing IRF-E sites and its mutants with different lengths. Then the cells were treated with or without 1200 U / ml IFN-a for additional 12 h ( 1000 U / ml) after 24 h of transfection, and the cell lysate was prepared and assayed for luci It was found that normal human liver expressed the mRNA of A3G. A3G mRNA expression in HuH-7 and HepG2 cells were up-regulated by IFN-αstimulation in a dose-dependent-dent manner. Western blot analysis showed that A3G protein expression was also enhanced by IFN-αstimulation. Sequence analysis showed the existence of putative sites of IFN regulatory factor element (IRF-E) in 5 ’region of A3G gene upstream the initiation codon. IFN-αstimulation results in 6- to 8-fold increase in luciferase activity in cells transfected with the plasmid containing IRF-E sites of the 5 ’downstream sequences, whereas luciferase activity did not change in cells transfected with the plasmid containing mutant IRF-E sites or without IRF-E sites. A3G expression was up-regulated by IFN-αstimulation in hepatoma cells and could be involved in host defense mechanisms against HBV. A3G expression was up-regulated by IFN-αstimulation in hepatoma cells and HBV may be involved in host defense mechanisms against HBV. ion codon plays an important role in this process.