Results: Overall meta-analysis indicated that -308A heterozygotes (GA) had 22% decreased risk of developing CHB with a borderline significance (OR = 0.78; 95% CI: 0.60-1.02; P = 0.065). For the -308A allele homozygotes (AA) and carriers (GA+AA), the pooled ORs both indicated a significantly decreased risk of CHB (OR = 0.39; 95% CI: 0.21-0.73; P = 0.003; and OR = 0.74; 95% CI: 0.57-0.96; P = 0.026, respectively) ( Table 1 ). In the subgroup analyses by ethnicity, significantly decreased risks were associated with -308 variant genotypes (GA and AA) in Mongoloid populations in all genetic models. However, no significant associations were found in Caucasoid. Conclusion: The meta-analysis suggests that the TNF--308A allele is a low-penetrant protective factor for chronic HBV infection, especially in Mongoloid. Aim: To define the potential role of PD-1/PD-Lpathway in different HBV infection status; we examined the expression of PD-1on CD8+ T cells in PBMC of patients with CHB and AEHB infection. Methods: The PD-1 level on CD8+ T lymphocytes and the number of HBV specific CD8+ T lymphocytes in patients and healthy controls were analyzed by flow cytometry. PCR was used to measure the serum HBVDNA levels. Results: The level of PD-1 expression on CD8+ T cells in CHB patients was higher than that in AEHB patients and healthy individuals. Compared to AEHB patients, lower frequency of HBV-specific CD8+ T cells was detected in CHB patients. There was an inverse correlation between the strength of HBV-specific CD8+ T-cell response and the level of PD-1 expression. Besides, there was a significant positive correlation between HBV viral load and the percentage of PD-1 expression on CD8+ T cells in CHB and AEHB subjects. However, PD-1 expression was not associated with ALT levels. Conclusion: Our results confirm previous reports that HBV specific CD8+ T-cell response in the peripheral blood is more intense in patients with AEHB than in CHB with persistent viral infection. Moreover, there is a negative correlation between the level of PD-1 and the intensity of virus specific CD8+ T cell response. observed in 10.9% of patients with a mean age of 51.8±12.9. The ethnic composition was 53.1% Chinese; 27.3% Malay; 14% indigenous Sabahans; 2.9% indigenous Sarawakians; 1.8% Indians and 0.8% others. Chinese patients were on average, older (mean 45.6±14.5 years), Indians patients had higher mean alanine transaminase and indigenous Sarawakian patients had the highest rate of cirrhosis (P<0.0001). During the study period, 20.7% of patients were on treatment and they were significantly older than those who were not on treatment (mean age 44.6 ± 14.5 vs 40.7 ± 14.3). Lamivudine was the first agent used in 86.9% of cases. Conclusions: In Malaysia, CHB remains a public health issue and significantly afflicts males in the productive age groups and of Chinese ethnicity. The observed differences among ethnic groups could point to different disease severity which needs to be addressed in the local treatment guideline and policy. Background/Aims: Liver stiffness measurement (LSM) has been validated for predicting fibrosis stage in patients with chronic hepatitis C. However, studies on LSM for chronic hepatitis B (CHB) are few, and the relationship between histologic findings and liver stiffness needs to be further elucidated. This study was conducted to assess the association of histologic activity on liver stiffness in addition to fibrosis in patients with CHB Methods: Thirty three patients who had taken liver biopsy and LSM at Korea University Ansan Hospital between March 2008 and October 2008 were enrolled. Necroinflammatory activity and fibrosis stage were assessed by Metavir system. Activity, fibrosis, and the sum of both score were included for the correlation analysis with LSM Results: Among 33 patients, 29 (87.9%) were male, and median values were as follows: age, 42 (20~54); AST, 49 IU/L (19~627); ALT, 62 IU/L (8~778); Total bilirubin, 1.03 mg/dL (0.4~2.39); LSM, 10.1 kPa (4.2~43.5). Fibrosis stages were F1 in 4 (12.1%), F2 in 9 (27.3%), F3 in 12 (36.4%), and F4 in 8 (24.2%) patients. Spearman correlation coefficient with LSM were 0.457 (p=0.008) for activity, 0.694 (p<0.001) for fibrosis stage, and 0.724 (p<0.001) for the sum of activity and fibrosis. In linear regression analysis, only the sum of activity and fibrosis remained to be significant. Conclusions: Not only fibrosis but also activity was an important factor for determining LSM for CHB. It would be more appropriate to consider both activity and fibrosis for interpretation of LSM in patients with CHB Background: HBeAg seroconversion is a key goal of CHB therapy. HBeAg kinetics may predict HBeAg seroconversion during treatment. We aim to develop a robust HBeAg quantitative method as the value of HBeAg quantitation is undefined and data is limited. Methods: We evaluated two commercially available qualitative HBeAg assays (Abbott Architect, Siemens Centaur) for their linear range and validated them against Paul-Ehrlich Institute (PEI) standards. HBeAg levels were determined from samples of untreated and telbivudine-treated CHB patients. Results: As a pre-requisite for quantitative use, the linear range for the Architect (0.5-43 PEIU/mL) and Centaur (0.05>5 PEIU/mL) assays were defined. Architect was selected for further investigation. HBeAg levels of 44 untreated patients (mean HBV-DNA 9.8 log10 copies/mL, mean ALT 166.7 IU/mL) varied from 0.4 to 1073.5 PEIU/mL (median 161.7 PEIU/mL). In 23 patients (mean HBV-DNA 9.9 log10 copies/mL, ALT 166 IU/mL) treated with telbivudine for 12 weeks, baseline HBeAg levels varied from 1.6 to 664 PEIU/mL (median 150.7 PEIU/mL). After 12 weeks of telbivudine treatment, median HBeAg level was 4.4 PEIU/mL, with 76% decline from baseline (median decline 95.1 PEIU/mL, range 1.4-657.6 PEIU/mL). Individual HBeAg decline from baseline varied but occurred in all patients and was not correlated to baseline or decline from baseline HBVDNA. Conclusion: HBeAg quantitation is feasible and robust with Architect HBeAg assay. HBeAg decline occurred in all telbivudine-treated patients, and was not correlated to HBVDNA. Whether the magnitude of HBeAg decline is predictive of future HBeAg seroconversion merits further investigation.