High Viral Load Does Not Necessarily Represent Significant Liver Damage in Patients with Chronic HBV Infection in Bangladesh M. Mahtab 1 , S. Rahman 1 , F. Akbar 2 , F. Karim 1 , A. Shrestha 1 , M. Khan 1 , M. Kamal 1 1 Bangabandhu Sheikh Mujib Medical University, 2 Toshiba General Hospital, Dhaka, Bangladesh Background: In general, it is assumed that patients with chronic hepatitis B virus (HBV) infection with high viral load exhibit increased liver damages. Treatment guidelines also emphasize on reducing viral load. These observations were mainly accumulated from developed countries. >80% chronic HBV carriers live in the developing nations, but little is known about relationship between HBV viral load and extent of liver damage in these countries. In this study, we addressed this issue. Methods: In this retrospective study we reviewed records of 306 CHB patients from our pool of 561 patients. All had high HBV DNA (>10 5 copies/ml). 62. 1% (190/306) were HBeAg +ve and 37.9% (116/306) HBeAg -ve. They were alsotested for anti-HCV and serum ALT. All underwent per-cutaneous liver biopsy. Results: 51.1% (97/190 ) HBeAg +ve patients with high HBV DNA had non-significant hepatic necro-inflammation (HAI-NI <7); this figure was 53.4% (62/116) in HBeAg -ve patients. Non-significant hepatic fibrosis (HAI-F <3) was observed in 75. 2% (143/190) and 69.8% (81/116) in HBeAg +ve and -ve patients respectively. None tested positive for HCV. Conclusion: Correlation doew not exist between viral load and liver damage in CHB in Bangladesh. Many with both HBeAg +ve and -ve CHB with high HBV DNA do not have significant hepatic necro-inflammation and fibrosis. Further study may be needed to find out influence of other factors on liver damages in CHB in Bangladesh. Most of these patients have not been characterized and treatment modalities have not been defined for them. Background/Aims: Expression of intrahepatic hepatitis B core antigen (HBcAg) is related to the immunopathogenesis of hepatitis B virus (HBV) infection. The role of HBV genotype and basal core promoter (BCP) mutation in expression of HBcAg was investigated. Methods: Seventy HBeAg-positive chronic hepatitis patients (genotype B in 52 and C in 18; BCP T1762/A1764 mutation in 16) were enrolled. Clinical, virologic and histologic features were compared with regard to localization and expression of intrahepatic HBcAg. The effects of HBV genotype and BCP T1762/A1764 mutation on the expression of HBcAg were further evaluated by in vitro assays. Results: Cytoplasmic, mixed cytoplasmic/nuclear, and nuclear localization of intrahepatic HBcAg were found in 38 (56.7%), 25 (37.3%) and 4 (6.0%), respectively. Fifty-eight (80.6%) of these patients expressed a high level of HBcAg. In multivariate analysis, cytoplasmic localization of HBcAg correlated only with low serum viral load (P=0.045) and BCP mutation (P=0.04). High expression level of HBcAg also correlated with high serum viral load (P=0.015) and BCP wild-type sequence (P=0.037). In vitro assays supported that HBV BCP mutant had lower subcellular expression of HBcAg compared with BCP wild-type strain. Conclusions: HBV BCP mutation and viral load but not genotype contributes to the expression of intrahepatic HBcAg.