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目的探讨HBV前S基因变异与疾病进展的关系。方法收集无症状携带者(ASC)、慢性肝炎(CH)、肝炎肝硬化(LC)、肝细胞癌(HCC)患者血清138份,PCR扩增前S区基因,聚合酶链反应-限制性片段长度多态性检测前S2起始码变异,聚丙烯酰胺凝胶电泳(PAGE)分析前S缺失变异,直接测序确定前C A1896、基本核心启动子(BCP)T1762/A1764变异。数据行χ~2检验。结果HCC、LC组前S缺失变异检出率分别为56.3%和42.9%,高于CH组的11.8%和ASC组的8.1%(P<0.01)。前S2起始码变异检出率在HCC(50.0%)、LC(37.1%)组亦较CH(5.9%)、ASC(0)组高。前S缺失、前S2起始码变异在HBeAg阴性组的检出率分别为37.5%和36.1%,高于HBeAg阳性组的19.7%和7.6%(P<0.01)。分析前S基因、T1762/A1764、A1896单独或联合变异在HCC、LC组和CH、ASC组的分布,Fisher精确检验表明,T1762/A1764和前S基因的联合变异是影响疾病进展、导致严重肝病的重要因素(P=0)。结论严重肝病患者前S基因变异发生率高,有T1762/A1764联合前S基因变异HBV感染者的肝病易进展。
Objective To investigate the relationship between HBV preS gene mutation and disease progression. Methods The serum samples of asymptomatic carriers (ASC), chronic hepatitis (CH), cirrhosis of liver (LC) and hepatocellular carcinoma (HCC) were collected from 138 patients. The gene of S region before PCR amplification, polymerase chain reaction - restriction fragment Length polymorphism was used to detect the variation of the start S2 codon before polyacrylamide gel electrophoresis (PAGE) analysis of the S deletion mutation, direct sequencing to determine the pre-C A1896, basic core promoter (BCP) T1762 / A1764 mutation. Data line χ ~ 2 test. Results The positive rate of S deletion mutation in HCC and LC group was 56.3% and 42.9% respectively, which was higher than 11.8% in CH group and 8.1% in ASC group (P <0.01). The mutation detection rate of pre-S2 start code was also higher in HCC (50.0%) and LC (37.1%) than CH (5.9%) and ASC (0). The former S deletion, the detection rate of pre-S2 start codon mutation in HBeAg-negative group was 37.5% and 36.1% respectively, higher than 19.7% and 7.6% in HBeAg-positive group (P <0.01). The distribution of pre-S gene, T1762 / A1764, A1896 alone or in combination in HCC, LC group and CH, ASC group was analyzed. Fisher exact test showed that the combined mutation of T1762 / A1764 and pre-S gene affected the progress of the disease and led to severe liver disease The important factor (P = 0). Conclusions The incidence of pre-S gene mutation in patients with severe liver disease is high, and liver disease with HBV infection of T1762 / A1764 combined with pre-S gene mutation is likely to progress.