Association of core promoter mutations of hepatitis b virus and viral load is different in HBeAg(+) and HBeAg(-) patients

Andi Utama, Marlinang Diarta Siburian, Sigit Purwantomo, Mariana Destila Bayu Intan, Tri Shinta Kurniasih, Rino A. Gani, Wenny Astuti Achwan, Arnelis, Syafruddin Ar Lelosutan, Benyamin Lukito, Tantoro Harmono, Nasrul Zubir, Julius, Soewignjo Soemohardjo, Laurentius M. Adrianto Lesmana, Ali Sulaiman, Susan Tai

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

Abstract

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(-) patientshad 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.

Original languageEnglish
Pages (from-to)708-716
Number of pages9
JournalWorld Journal of Gastroenterology
Volume17
Issue number6
DOIs
Publication statusPublished - 14 Feb 2011

Keywords

  • Hepatitis B e antibody
  • Hepatitis B e antigen
  • Hepatitis B virus
  • Indonesia
  • Precore/core promoter mutations
  • Viral load

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