Results: different treatment of HBV -DNA effect of the existence of significant differences; P> 0.01, the performance of different types of asymptomatic carriers negative rate of HBV-DNA there is a significant difference; P> 0.01, as well as the performance of the different types of asymptomatic carriers continued application A treatment plan presented HBV-DNA rebound rate there is a significant difference; P> 0.01, Conclusion: HBV-DNA and non-specific immune responses in response to the lower capacity, anti-HBV therapy is not associated with non-specific immune response capacity or improve Is the anti-HBV drugs alone can not solve the asymptomatic carriers in anti-HBV therapy where the cause of the problem, solve the asymptomatic carriers in the anti-HBV treatment although the need for anti-HBV drugs with non-specific immune activation synchronous drugs on the basis of the Joint application , but the simultaneous combination of two drugs rather than as a result of HBeAg and HBV-DNA can HBeAg-positive asymptomatic carriers receive HBV-DNA negative effect of the results. Background: Adefovir dipivoxil (adefovir) effectively inhibits both wild-type and lamivudine (LAM)-resistant hepatitis B virus (HBV) replication and resistance to this drug is infrequent compared with LAM. In this study, we tried to identify factors affecting the emergence of resistant mutants after adefovir monotherapy in LAM-resistant chronic hepatitis B (CHB) patients. Methods: The subjects were 87 CHB patients with LAM-resistance who had received adefovir for more than 12 months (range 12-39 months). The initial viral response (IVR) was defined as HBV DNA <4.0 log copies/mL. The adefovir resistant mutant was assayed at baseline and every 6 months during adefovir administration. Results: IVR was observed in 38% of patients. The cumulative emergence rates of adefovir resistance were 2.6% at 6 months, 10.4% at 1 year, 14.6% at 2 years and 21% at 3 years. In univariate analysis, factors contributing to the emergence of adefovir resistant virus were baseline HBV DNA > 6 log copies/mL (P=0.003) and IVR (P<0.0001). The presence of precore mutation and type of YMDD mutants were not related. In multivariate analysis, only IVR was an independent factors affecting the emergence of adefovir resistant virus (P<0.0001). Conclusion: IVR is a useful predictor for emergence of adefovir resistant mutants after adefovir monotherapy in LAM-resistant CHB patients. For IVR-negative patients, the change of therapeutic options such as add-on LAM or switch to other drugs should be considered because of the high incidence of the emergence of adefovir resistant mutants. Background: Elevated HBV DNA is strongly associated with the risk of disease progression. This study investigated the early viral suppression effects of ETV and LVD in nucleoside-naïve Chinese patients with active HBeAg (+) CHB.