Conclusions: Long-term ETV therapy in nucleoside-naïve CHB patients results in durable virologic suppression, continued histologic improvement and regression of fibrosis/cirrhosis. Precore (PC, G1896A) and basal core promoter (BCP, A1762T and G1764A) mutations of HBV are important for predicting the risk of hepatocellular carcinoma (HCC). We developed a new mass spectrometry-based assay using restriction fragment mass polymorphism (RFMP) to detect A1896 and T1762/A1764 mutations, and applied it to analyze their clinical significance in type B liver diseases (N=336), including 35 HCCs, 118 liver cirrhosis (LC), 157 chronic hepatitis B (CHB), and 25 HBsAg-positive with low level viremia (inactive HBsAg carrer, IHC). We devided patients into 4 major groups according to the presence of wild (W) or mutant (M) genes in BCP/PC regions; W/W, W/M, M/W and M/M gene types. Each proportion was 9.5%, 3.6%, 41.4% and 23.5%, respectively. Mixed infection (X) was also found as minority; 4 W/X, 28 M/X, 15 X/W, 4 X/M and 13 X/X. Disease distributions (HCC, LC, CHB and IHC) in each group were as follows; [W/W (n=32)] 3.1%-6.3%-90.6%-0; [W/M (n=12)] 0-16.7%-58.3%-25%; [M/W (n=139)] 9.4%-42.5%-46%-2.2%; [M/M (n=79)] 11.4%-45.5%-20.1%-13.9%. These results suggest that, in Korea where only genotype C has been identified, BCP dual mutation is predominant (>73.2%), while BCP wild alone is only 13.1%. Especially, A1896 mutation alone without BCP mutation (W/M type) is uncommon, while BCP mutation alone without A1896 mutation (M/W type) is most common. It might be suggested that prognosis of wild type in BCP and PC region (W/W type) is much better than that of M/W or M/M types. Background/Aims: Entecavir is a potent inhibitor of HBV DNA polymerase, which has been shown to be safe and effective for the treatment of chronic hepatitis B (CHB) patients. The aim of this study was to evaluate the virologic, biochemical, and serologic responses of entecavir through 1 year in CHB patients. Methods: From 2007 May to 2008 October, we reviewed 82 patients (mean age 46±12 years, male:female=57:25) who were diagnosed as CHB patients (HBeAg (+) 64). Forty-seven patients (57.3%) had been treated with 0.5 mg of entecavir and 35 (42.7%) with 1 mg of entecavir, respectively. Mean follow-up period was 25±17 weeks. HBV DNA was quantified by bDNA assay with a lower limit of detection of 141,500 copies/mL.