乙型肝炎肝硬化病人的乙型肝炎病毒C基因启动子和前C基因变异及其对e抗原系统的影响  

Mutations in the core promoter and pre-core gene of hepatitis B virus and its influence on the e-antigen system in liver cirrhosis patients with hepatitis B

作　　者：侯旭芬 张汉荣[2] 刘新钰[2] 孙梅[2] 

机构地区：[1]江苏省靖江市肿瘤医院,江苏靖江214515 [2]东南大学医学院附属南京市第二医院,江苏南京210003

出　　处：《世界感染杂志》2007年第4期285-287,共3页World Journal of Infection

摘　　要：目的研究乙型肝炎肝硬化病人血清的乙型肝炎病毒（HBV）C基因启动子（CP）和前C基因变异。方法通过DNA扩增、基因序列分析检测34例活动性肝硬化和75例慢性乙肝病人血清的HBV CP和前C基因序列，通过微粒子发光法定量检测血清中HBeAg的含量，及通过荧光定量PCR技术定量检测血清中的HBV DNA。结果（1）CP双变异（nt 1762A→T和1764G→A）在肝硬化（LC）组的发生率显著高于慢性乙型肝炎（CH）组（76．5％vs48．0％）；前C终止变异（nt1896G→A）则在LC组和CH组的发生率无显著差异（35.3％vs26．7％）。（2）CP双变异虽使HBeAg表达显著下降，但幅度较小；与对照组相比，CP双变异组的HBeAb阳性率也无明显升高；前C终止变异则大幅度影响HBeAg表达，显著增高HBeAg／HBeAb转换率；终止变异联合双变异组的HBeAg含量及HBeAb阳性率同终止变异组相似。（3）HBeAb阳性LC组的前C终止变异的发生率显著高于HBeAb阴性LC组（75．0％vs5．6％）；而CP双变异则在两组LC中无明显差异（75．0％vs77．8％）。结论CP双变异可能与乙型肝炎肝硬化发病机制有关；前C终止变异则与肝硬化病人的HBeAg／HBeAb转换有关。Objective To study mutations in the core promoter （CP） and pre-core gene of hepatitis B virus （HBV） in patients with liver cirrhosis and their relationship with serum HBeAg and anti- HBe. Metheds CP and pre-core gene were sequenced directly from sera of 34 cases of patients with liver cirrhosis （LC） and 75 cases of patients with chronic hepatitis B（CH）, then detected by the polymerase chain reaction. Results The double mutations in CP （A-to-T at nt 1762 and G-to- A at nt 1764） were observed in 26 of 34 cases of patients with LC （76.5%） and in 36 of 75 cases of patients with CH （48.0%）, the difference of which was significant. The difference in the prevalence of pre-core mutation （G-to- A at nt 1896） between LC group and CH group was not significant （35.5% vs 26.7%）. The prevalence of pre-core mutation in anti-HBe-positive patients with LC was significantly higher than that of anti-HBe-negative patients with LC （75.0% vs 5.6%）. Conclusion CP mutations are probably related to the mechanism of liver cirrhosis. Pre-core mutation significantly blocks synthesis of HBeAg.

关 键 词：肝炎病毒 乙型 肝硬化 C基因启动子 前C基因 变异 聚合酶链反应 

分 类 号：R373.21[医药卫生—病原生物学]