AIM:To identify the prevalence of hepatitis B e antigen (HBeAg) and to assess the association of hepatitis B virus (HBV) core promoter mutations and viral load in Indonesian patients.METHODS:Sixty-four patients with chronic hepatitis,65 with liver cirrhosis and 50 with hepatocellular carcinoma were included in this study.HBeAg and hepatitis B e antibody (HBeAb) tests were performed using enzyme-linked immunosorbent assay and the mutations were analyzed by sequencing.Viral load was measured by real-time polymerase chain reaction.RESULTS:Of 179 patients,108 (60.3%) were HBeAg(-) and 86 (79.6%) of these HBeAg(-) patients had been seroconverted.The A1896 mutation was not found in HBeAg(+) patients,however,this mutation was detected in 70.7% of HBeAg(-) patients.This mutation was frequently found when HBeAg was not expressed (87.7%),compared to that found in HBeAg seroconverted patients (65.1%).The A1899 mutation was also more prevalent in HBeAg(-) than in HBeAg(+) patients (P=0.004).The T1762/A1764 mutation was frequently found in both HBeAg(+) and HBeAg(-) patients,however,the prevalence of this mutation did not significantly differ among the two groups (P=0.054).In HBeAg(+) patients,the T1762/A1764 mutation was correlated with lower HBV DNA (P < 0.001).The A1899 mutation did not correlate with HBV DNA (P=0.609).In HBeAg(-) patients,the T1762/A1764 mutation alone was not correlated with HBV DNA (P=0.095),however,the presence of either the T1762/A1764 or A1896 mutations was associated with increased HBV DNA (P < 0.001).CONCLUSION:The percentage of HBeAg(-) patients is high in Indonesia,and most of the HBeAg(-) patients had been seroconverted.The A1896 mutation was most likely the major cause of HBeAg loss.The T1762/A1764 mutation alone was associated with lower viral loads in HBeAg(+) patients,but not in HBeAg(-) patients. AIM: To identify the prevalence of hepatitis B e antigen (HBeAg) and to assess the association of hepatitis B virus (HBV) core promoter mutations and viral load in Indonesian patients. METHODS: Sixty-four patients with chronic hepatitis, 65 with liver cirrhosis and 50 with hepatocellular carcinoma were included in this study. HBEAg and hepatitis B e antibodies (HBeAb) tests were performed using enzyme-linked immunosorbent assay and the mutations were analyzed by sequencing. Viral load was measured by real-time polymerase chain reaction. Of 179 patients, 108 (60.3%) were HBeAg (-) and 86 (79.6%) of these HBeAg (-) patients had been seroconverted. The A1896 mutation was not found in HBeAg (+) patients, however, this mutation was detected in 70.7% of HBeAg (-) patients. This mutation was frequently found when HBeAg was not expressed (87.7%), compared to that found in HBeAg seroconverted patients (65.1%). The A1899 mutation was also more prevalent in HBeAg (- ) than in HBeAg (+) patients (P = 0.004) .The T1 The prevalence of this mutation did not significantly differ among the two groups (P = 0.054). In HBeAg (+) patients, the T1762 The A1899 mutation was not correlated with HBV DNA (P = 0.609). In HBeAg (-) patients, the T1762 / A1764 mutation alone was not correlated with HBV DNA (P < P = 0.095), however, the presence of either the T1762 / A1764 or A1896 mutations was associated with increased HBV DNA (P <0.001) .CONCLUSION: The percentage of HBeAg (-) patients is high in Indonesia, and most of the HBeAg (-) patients had been seroconverted. The A1896 mutation was most likely the major cause of major cause of HBeAg loss. T1762 / A1764 mutation alone was associated with lower viral load in HBeAg (+) patients, but not in HBeAg (-) patients.