Published online Mar 21, 2016. doi: 10.3748/wjg.v22.i11.3268
Peer-review started: November 8, 2015
First decision: November 27, 2015
Revised: December 14, 2015
Accepted: December 30, 2015
Article in press: December 30, 2015
Published online: March 21, 2016
Processing time: 126 Days and 22.2 Hours
AIM: To investigate the frequency of mutations in pre-core (pre-C) and basic core promoter (BCP) regions of hepatitis B virus (HBV) from Shanxi Province, and the association between mutations and disease related indexes.
METHODS: One hundred chronic hepatitis B patients treated at Shanxi Province Hospital of Traditional Chinese Medicine were included in this study. PCR-reverse dot blot hybridization and mismatch amplification mutation assay (MAMA)-PCR were used to detect the mutations in the HBV pre-C and BCP regions. HBV DNA content and liver function were compared between patients with mutant HBV pre-C and BCP loci and those with wild-type loci. The consistency between PCR-reverse dot blot hybridization and MAMA-PCR for detecting mutations in the HBV pre-C and BCP regions was assessed.
RESULTS: Of the 100 serum samples detected, 9.38% had single mutations in the pre-C region, 29.17% had single mutations in the BCP region, 41.67% had mutations in both BCP and pre-C regions, and 19.79% had wild-type loci. The rates of BCP and pre-C mutations were 65.7% and 34.3%, respectively, in hepatitis B e antigen (HBeAg) positive patients, and 84.6% and 96.2%, respectively, in HBeAg negative patients. The rate of pre-C mutations was significantly higher in HBeAg negative patients than in HBeAg positive patients (χ2 = 26.62, P = 0.00), but there was no significant difference in the distribution of mutations in the BCP region between HBeAg positive and negative patients (χ2 = 2.43, P = 0.12). The presence of mutations in the pre-C (Wilcoxon W = 1802.5, P = 0.00) and BCP regions (Wilcoxon W = 2906.5, P = 0.00) was more common in patients with low HBV DNA content. Both AST and GGT were significantly higher in patients with mutant pre-C and BCP loci than in those with wild-type loci (P < 0.05). PCR-reverse dot blot hybridization and MAMA-PCR for detection of mutations in the BCP and pre-C regions had good consistency, and the Kappa values obtained were 0.91 and 0.58, respectively.
CONCLUSION: HBeAg negative patients tend to have HBV pre-C mutations. However, these mutations do not cause increased DNA copies, but associate with damage of liver function.
Core tip: There is no exact evidence about the frequency of mutations in hepatitis B virus (HBV) pre-C and basic core promoter (BCP) regions of HBV in Shanxi Province and the correlation between mutations and disease-related indicators. Here, we found that the frequency of pre-C mutations was higher in hepatitis B e antigen (HBeAg) negative patients, and liver function parameters AST and GGT in the mutation group were higher than those in the wild-type group; however, DNA replication did not increase in the presence of HBV pre-C and BCP mutations. Taken together, HBeAg-negative patients tend to have HBV pre-C mutation. However, these mutations do not cause increased DNA copies, but associate with liver function damage.