Background/Aim: To evaluate the efficacy and safety of entecavir treatment in patients with HBeAg-positive chronic hepatitis B who had not previously received a nucleoside analogue. Methods: Fifty-five patients received 48-week entecavir 0.5mg/d therapy. Serum HBV DNA load was measured with quantitative real-time-PCR. Alanine aminotransferase (ALT) activity, HBeAg, anti-HBe-antibodies, HBV DNA level in serum were evaluated at baseline, week 2, 12, 24 and 48 during therapy. Evaluation of safety and tolerance was based on clinical adverse events and laboratory analyses. Results: HBV DNA levels declined sharply by around 3 log10 copies/mL during the first two weeks, with a highly significant reduction (p<0.0001) at week 2 and thereafter, as compared to those at baseline; 31%, 51% and 78% of the patients had undetectable serum HBV DNA levels at week 12, 24 and 48 respectively. Highly significantly decreasing serum ALT (p<0.0001) occurred during the first 2 weeks of the study. At week 48, ALT levels were normalized in 84% of the patients. HBeAg seroconversion (HBeAg negative, HBeAb positive) was achieved in 7.3% and 14.5% of patients by 24 and 48week. At the end of 24 th and 48 th weeks, complete response (ALT normalization and HBV DNA and HBeAg loss) was observed in 11% and 15%, respectively. There was no evidence of drug resistance or adverse effect in CHB patients treated for up to 48 weeks. Conclusion: Entecavir treatment through 48 weeks was well tolerated and resulted in continued benefit for patients with HBeAg-positive chronic hepatitis B. Aim: To assess the associations of single nucleotide polymorphisms of the MxA gene promoter and sustained treatment response of chronic hepatitis B or C patients with interferon treatment by meta-analysis of individual dataset from all studies published till date. Methods: To clarify the impact of MxA gene promoter polymorphisms on sustained treatment response of chronic hepatitis B or C patients with interferon treatment, we performed a meta-analysis of the published data from eight studies comparing the frequencies of MxA gene promoter polymorphisms at nt -88 G/G, -88 G/T, -88 T/T and nt -123 C/C, -123 C/A , -123 A/A alleles in individuals with interferon treatment. As we identified the heterogeneity between studies, summary statistical data were calculated based on a random-effect model. Results: The sustained treatment response rate was higher in patients with the nt -88 G/T and nt -123 C/Aalleles in the MxA promoter SNP . The Meta-analyses yielded summary estimatesodds ratio (OR) were 2.07 [95%CI (1.58, 2.7), P <0.00001] and 1.9 [95%CI (1.32, 2.73), P =0.0006] of the nt -88 G/T and nt -123 C/A alleles, respectively. Conclusion: MxA gene promoter polymorphisms at nt -88 G/T and nt -123 C/A may be useful as a marker to predict the sustained treatment response of chronic hepatitis B or C patients with interferon treatment, and further investigation regarding their real significance is warranted in a large series of patients. Background: To determine whether HBV with the same characteristics causes dissimilar mutations in different hosts. Methods: Full-length HBV genome was amplified and linked with pMD T18 vector. Positive clones were selected by double-restriction endonuclease digestion (EcoRI and HindIII) and PCR. Twenty seven clones were randomly selected from an asymptomatic mother [at two time points: 602 (1 d) and 6022 (6 mo)] and her son [602 (S)]. BioEditor, Clustal X and MEGA software were used to perform phylogenetic and mutational analysis. Potential immune epitopes were determined by the Stabilized Matrix Method (SMM), SMM-Align Method and Emini Surface Accessibility Prediction. Result: All of the 27 sequences were genotype C, the inner-divergence for the mother and son was 0%-0.8%.13 specific nucleotides differed from the other pubished genotype C isolates were co-exist in the mother and her son. AA 1-11 deletion in preS1 was the dominant mutation in the mother (14/18). The 1762T/1764A double mutation existed in all clones of the mother, 3 of them were also coupled with G1896A mutation, but none were found in the son. 17 bp deletion starting at nucleotide 2330 was the major mutation (5/9) in the son, which caused seven potential HLA class I epitopes and one B cell epitope deletion, and produced a presumptive new start codon, downstream from the original one of the P gene. Conclusion: The son was infected HBV from his mother, and discrepant mutation occurred in the mother and her son during infection. Background/aims: Nucleos(t)ide analogues have been recognized as an effective treatment for chronic hepatitis B. This randomized, double-blind trial compared the efficacy and safety of telbivudine and lamivudine after 104-week therapy in patients with compensated chronic hepatitis B in Taiwan. Methods: We analyzed 114 Taiwanese patients from GLOBE trial receiving telbivudine 600mg (n=58) or lamivudine 100mg (n=56) once daily for 104 weeks. The primary efficacy endpoint was therapeutic response with serum HBV DNA <5 log10 copies/ml and either hepatitis B e antigen (HBeAg) loss or alanine aminotransferase (ALT) normalization. Results: The therapeutic response at week 104 was 74.8% in telbivudine group versus 50% in lamivudine group (p=0.005). More patients with telbivudine achieved nondetectable serum HBV DNA (<300 copies/ml) (p=0.024) and ALT normalization (p=0.021) at the end of treatment. The cumulative resistant rate was significantly lower in those with telbivudine treatment (p=0.0032). The rate of HBeAg seroconversion was comparable in both groups (p=0.407). Although a lower percentage of patients in lamivudine group (83.9%) reported adverse events than those in telbivudine group (89.7%), the difference was not significant. Conclusions: Telbivudine demonstrates a significantly greater efficacy and a lower resistant rate than lamivudine in treatment of chronic hepatitis B in Taiwan. Background: Tumor necrosis factor-(TNF-) plays a pivotal role in the viral clearance and host immune response to HBV, and the capacity for TNF-production in individuals is influenced by a major genetic component. The studies of TNF--308 gene promoter polymorphism in chronic HBV infection have reported apparently conflicting results. Objective: To derive a more precise estimation of the relationship between the polymorphism of TNF--308 gene promoter and chronic HBV infection. Method: Meta-analysis was done of 22 case-control studies in relation to TNF--308 gene promoter, involving a total of 4338 chronic HBV infection cases and 3013 controls. The pooled odds ratios (ORs) for the risk associated with the genotypes of GA, AA, and GA+AA (A-allele carriers) compared with the GG genotype were calculated.