[Significance of the double mutations of C1673T/C1799G in HBV C promoter]

Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 2012 Oct;26(5):321-3.
[Article in Chinese]

Abstract

Objective: To explore the biological and clinical significance of the double mutations of C1673T/C1799G in HBV C promoter (CP).

Methods: Totally 136 patients were enrolled, including 25 asymptomatic carriers (AsC), 38 patients with chronic hepatitis B (CHB), 24 patients with chronic severe hepatitis B (CSHB), 36 cases with liver cirrhosis (LC) and 13 cases with hepatocellular carcinoma (HCC). HBV subgenotypes and mutations in CP of all samples were determined by nested-PCR and direct nucleotide sequence analysis. The C to T mutation at nucleotide 1673 and C to G at nucleotide 1799 were analyzed in different subgenotypes, and the relationships of C1673T/C1799G double mutations with HBV replication, the expression of HBeAg, and with the severity of liver disease after chronic HBV infection were studied.

Results: Of the 136 patients, 110 were subgenotype Ba, 1 was Bj, 7 were C1, and 18 were C2. C1673T/C1799G double mutations in Ba were determined in 106 (96. 4%) samples, which was significantly higher than in C1 (14.3%) and C2 (12.5%) subgenotype (P < 0.0001). In contrast to non-mutation group, HBV DNA content in mutation group had no significant difference (P > 0.05). The prevalence of the mutation was lower in HBeAg positive patients (71.4%) than in HBeAg negative patients (87.5%) (P < 0.05). The frequencies of the double mutations were not significantly different among ASC, CHB, CSHB, LC and HCC groups (P > 0.05).

Conclusion: In Ba subgenotype, double mutations of C1673T/C1799G is much popular than in C1 and C2; the mutation has no effect on HBV replication, and may not be associated with the outcome of chronic HBV infection.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Female
  • Genotype
  • Hepatitis B e Antigens / analysis
  • Hepatitis B virus / genetics*
  • Hepatitis B, Chronic / virology
  • Humans
  • Male
  • Middle Aged
  • Mutation*
  • Promoter Regions, Genetic*

Substances

  • Hepatitis B e Antigens