母婴传播母子体内乙型肝炎病毒复制与C区启动子变异的关系  

Relationship between the different replication status of HBV and mutations in core promoter in mother and children infected by mother-to-infant transmission

作　　者：许红梅[1] 任红[1] 卿玉玲[1] 彭明利[1] 凌宁[1] 

机构地区：[1]重庆医科大学病毒性肝炎研究所,400010

出　　处：《中华肝脏病杂志》2002年第5期358-361,共4页Chinese Journal of Hepatology

基　　金：国家自然科学基金资助(396-30280)

摘　　要：目的 了解母婴传播后母子体内 HBV复制程度差异与 C区启动子变异的关系。方法 对 8对复制程度不同的HBV C区启动子基因进行聚合酶链反应（PCR）,应用TA克隆技术构建重组质粒pGEM—CP,每例患者选2个双酶切鉴定正确的克隆测序并分析。结果 HBV复制状态,子高母低组平均变异数于为5.33±1.53,母为9.33±3.06;子低母高组于为8.25±4.27,母为5.00±1.41。母子低复制者C区启动子变异数及变异位点数明显高于高复制者,变异主要集中在BCP和Kunitz类丝氨酸蛋白序列区域,而同复制状态下母子间差异不大。结论母婴传播后母子体内HBV低复制状态与C区启动子变异有关,可能与机体的生长发育状态无关。Objective To understand the relationship between the different replication status of HBV and mutations in core promoter in mother and child infected by mother-to-infant transmission. Methods Core promoter was amplified by PCR and cloned into pGEM-T vector with T-A cloning technique. The recombinant plasmid pGEM-PreS/S was confirmed by digestion with restriction enzyme Apa I and Sac I . Two clones were selected to sequence each patient. Results Every pair of mother and child had same serotype and genotype and the homology of nucleotides encoding 'a' determinant was 98-100%. The number of mutations in core promoter in patients with high replication status was more than that of low replication status. Mutations were distributed in BCP and Kunitz-type serine protease inhibitor region mainly. This difference was not associated with mother or child. Conclusions The different replication status of HBV is caused by mutations in core promoter in mother and child infected by mother-to-infant transmission and seems not to be associated with the development status.

关 键 词：乙型肝炎病毒 母婴传播 复制 C区启动子 变异 乙型肝炎 

分 类 号：R512.62[医药卫生—内科学]