Prevalence of the precore G1896A mutation in Chinese patients with e antigen negative hepatitis B virus infection and its relationship to pre-S1 antigen

Abstract

This study investigated the prevalence of the precore G1896A mutation in Chinese patients with hepatitis B e antigen (HBeAg) negative HBV infection and its relation to serum HBV pre-S1 antigen. The overall prevalence of the precore G1896A mutation was 72.6% in HBeAg-negative Chinese patients with detectable serum HBV DNA. The prevalence of the precore G1896A is significantly higher in Chinese HBeAg-negative patients with chronic hepatitis B than that in inactive HBV carriers with detectable serum HBV DNA. Serum pre-S1 and the precore G1896A mutation were simultaneously detected in most of Chinese HBeAg-negative patients. In most instances, HBeAg-negative chronic hepatitis B is a result of HBV variants in the precore or core promoter region. The HBeAg is encoded by the core gene, which is divided into the precore (PC) region and the core region by two in-frame initiating ATG codons. Transcription of these open reading frames produces the pregenomic RNA that is essential for HBV replication and the PC RNA that translates into HBeAg, which is secreted into the serum (22). Variations

HBeAg-negative Patients with Chronic Hepatitis B Virus Infection and Normal Alanine Aminotransferase: Wait or Treat?

“…In recent years, studies have confirmed that some HBeAg-negative patients may not express the e antigen because of pre-C region mutations and other reasons, but their DNA is still duplicated at a high level. 16 The results of a study by Zhuang et al . 11 indicated that for HBeAg-negative patients with chronic HBV infection and normal ALTs, the proportion of liver inflammation or fibrosis in those with HBV DNA ≥2000 IU/mL significantly exceeded the proportion of those with HBV DNA <2000 IU/mL (58.5% vs. 27.1% and 67.9% vs. 46.2%, p <0.01).…”

Low-level viremia in nucleoside analog-treated chronic hepatitis B patients

“…Furthermore, a study from China showed that 72.60% of patients with positive HBV DNA and negative HBeAg had pre-C mutations. [ 26 ] These patients may not be real inactive carriers, but they need to be considered for treatment. Especially for HBeAg-negative patients with ALT level fluctuations, the indications should be considered to be relaxed for antiviral therapy because clinical long-term ALT monitoring is difficult.…”

“…This phenomenon may mask some patients’ need for treatment, resulting in disease progression. Furthermore, a study from China showed that 72.60% of patients with positive HBV DNA and negative HBeAg had pre-C mutations [26] . These patients may not be real inactive carriers, but they need to be considered for treatment.…”