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

• Main Author: LEI Man
• Format: Article
• Language: zho
• Published: Editorial Department of Journal of Clinical Hepatology 2014-06-01
• Series: Linchuang Gandanbing Zazhi
• Subjects: hepatitis B; chronic; liver cirrhosis; carcinoma; hepatocellular; point mutation
• Online Access: http://www.lcgdbzz.org/qk_content.asp?id=5902&ClassID=42414109
• ISSN: 1001-5256; 1001-5256

ObjectiveTo study the relationship between hepatocarcinogenesis and the mutation in X gene among patients with chronic hepatitis B virus (HBV) infection, such as chronic hepatitis B (CHB), liver cirrhosis (LC) and primary liver cancer (PLC). MethodsThe serum samples from 89 patients with chronic HBV infection who visited the Second Affiliated Hospital of Chongqing Medical University from 2011 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. ResultsAll 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 patients 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 genotype 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). ConclusionThe BCP double mutation and T-base deficiency at nt1821 site may play important roles in the development of PLC.