BACKGROUND:It has been shown that telomerase activ ty and hepatitis B virus (HBV) replication are closely asso ciated with cell cycle. This study aimed to further investi gate the effects of cell cycle on telomerase activity and on HBV replication. METHODS: Human hepatoma cells transfected with HBV DNA ( HepG2 2. 2. 15 cell line) were treated respectivel with serum deprivation, all-trans retinoic acid ( RA) dimethyl sulfoxide (DMSO), or sodium butyrate. The cel cycle of HepG2 2.2.15 cells was analyzed by flow cytome try. The telomerase activities of the cells were detected by TRAP-PCR-ELISA. HBV DNA in culture medium was as sayed by a fluorescent quantitative PCR assay and a semi quantitative dot blot hybridization technique. HBsAg and HBeAg in culture media were quantitatively examined by an ELISA assay. RESULTS: Treatments with serum deprivation, RA, DM SO, or sodium butyrate inhibited the proliferation o HepG2 2.2.15 cells and led to cell arrest in the G0/G1 phase of cell cycle. The percentage of the G0/G1 phase in the groups of sodium butyrate, DMSO, RA and serum-free was 85.2%, 71.9%, 68.3% and 65.2% , respectively, but in the control group, 43.1% (P<0.01). The activities of te lomerase of the cells were also significantly inhibited by 82.8%, 74.6%, 76.1% and 69.4% respectively. In addi tion, HBV replication of the HepG2 2. 2. 15 cells remark ably increased as shown by the contents of HBV DNA, HBsAg and HBeAg in the culture media of the cells treated with sodium butyrate, DMSO, RA or serum deprivation (P<0.01). The amounts of HBV DNA in the groups o sodium butyrate, DMSO, RA, serum deprivation and con trol were 6.7 ×106, 4.8×106, 4.4 ×106 , 5.1 ×106 and 1.2 × 106 copies/ml, respectively (P <0.01). Telomerase was ex- pressed mainly in the cells in S phase. HBV replication in- creased in quiescent cells (G0/G1 phase), and decreased in proliferating phase (S phase). CONCLUSION: The current data approve that HBV repli- cation is associated with the cellular proliferative activity. BACKGROUND: It has been shown that telomerase activ ty and hepatitis B virus (HBV) replication are closely asso ciated with cell cycle. This study aimed to further investi gate the effects of cell cycle on telomerase activity and on HBV replication. METHODS: Human hepatoma The transfected with HBV DNA (HepG2 2. 2. 15 cell line) were treated with l with serum deprivation, all-trans retinoic acid (RA) dimethyl sulfoxide (DMSO), or sodium butyrate. The cel cycle of HepG2 2.2.15 cells was analyzed by flow cytome try. The telomerase activities of the cells were detected by TRAP-PCR-ELISA. HBV DNA in culture medium was as say by a fluorescent quantitative PCR assay and a semi quantitative dot blot hybridization technique. HBsAg and HBeAg in culture media were quantitatively examined by an ELISA assay. RESULTS: Treatments with serum deprivation, RA, DM SO, or sodium butyrate inhibited the proliferation o HepG2 2.2.15 cells and led to cell arrest in the G0 / G1 phase of cell cycle. percentage of the G0 / G1 phase in the groups of sodium butyrate, DMSO, RA and serum-free was 85.2%, 71.9%, 68.3% and 65.2%, respectively, but in the control group, 43.1% (P <0.01). The activities of te lomerase of the cells were also significantly inhibited by 82.8%, 74.6%, 76.1% and 69.4% respectively. In addi tion, HBV replication of the HepG2 2. 2. 15 cells remark ably increased as shown by the contents of HBV DNA, HBsAg and HBeAg in the culture media of the cells treated with sodium butyrate, DMSO, RA or serum deprivation (P <0.01). The amounts of HBV DNA in the groups o sodium butyrate, DMSO, RA, serum deprivation and con Telomerase was ex- pressed mainly in the cells in S phase. HBV replication-creased (p <0.01) in quiescent cells (G0 / G1 phase), and decreased in proliferating phase (S phase). CONCLUSION: The current data approve that HBV repli cation is associated with the cellular pr oliferative activity.