Study of HBV-X gene mutation among patients with HBV-related chronic hepatitis,liver cirrhosis,and primary liver cancer
10.3969/j.issn.1001-5256.2014.06.013
- VernacularTitle:慢性乙型肝炎、乙型肝炎肝硬化及原发性肝癌患者HBV-X基因突变分析
- Author:
Man LEI
;
Song HE
- Publication Type:Journal Article
- Keywords:
hepatitis B,chronic;
liver cirrhosis;
carcinoma,hepatocellular;
hepatitis B virus;
point mutation
- From:
Journal of Clinical Hepatology
2014;30(6):531-536
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the relationship between hepatocarcinogenesis and the mutation in X gene among patients with chronic hepa-titis B virus (HBV)infection,such as chronic hepatitis B (CHB),liver cirrhosis (LC)and primary liver cancer (PLC).Methods The serum samples from 89 patients with chronic HBV infection who visited the Second Affiliated Hospital of Chongqing Medical University from 201 1 to 2013 were collected.PCR was used to amplify the X gene of HBV DNA extracted from the serum samples.After sequencing,the HBV-X genome was compared with those reported in GenBank to find the variable sites and variant forms.Chi -square and one -way ANOVA were used for the statistical analysis afterwards,whereas genotypes were determined by the genotyping tool of the National Center for Biotechnology Information.Results All patients were genotype B or C.Among HBeAg-positive patients,46.2% were genotype B,and 53.8% were genotype C;among HBeAg-negative patients,81.2%were genotype B,and 18.8%were genotype C (P=0.001).PLC pa-tients had a significantly higher risk of mutation in the basic core promoter (BCP)region than the CHB and LC groups (69.2%vs 34.4%and 61.3%,P<0.05);in addition,an evident T-base deficiency was observed at nt1821 site (88.5% vs 53.1% and 71%,P=0.014).Among CHB and LC patients,those with genotype C had a significantly higher risk of BCP double mutation than those with geno-type B (61.5%vs 15.8%,P=0.007;83.3%vs 47.4%,P=0.045).The incidence of BCP double mutation was significantly higher in the low-viral load group (≤106 copies/ml)than in the high-viral load group (>106 copies/ml)(81.3% vs 47.9%,P=0.015). Conclusion The BCP double mutation and T-base deficiency at nt1821 site may play important roles in the development of PLC.
