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

作　　者：Hong-Mei Xu Yu-Ling Qing Ming-Li Peng Ning Ling Hong Ren the Research Institute of Viral Hepatitis, Chongqing Medical University, Chongqing 400010, China 

出　　处：《Hepatobiliary & Pancreatic Diseases International》2003年第4期557-561,共5页国际肝胆胰疾病杂志（英文版）

基　　金：This study was supported by a grant from the National Natural Science Foundation of China (No. 39630280).

摘　　要：OBJECTIVE: To study the relationship between the different replication status of hepatitis B virus (HBV) and mutations in the core promoter (CP) in mother and her child infected by mother-to-infant transmission. METHODS: The core promoter was amplified by PCR and cloned into pGEM-T vector with the T-A choning technique. The recombinant plasmid pGEM-CP was confirmed by digestion with restriction enzyme Apa I and Sac I. Two clones were selected to be sequenced in 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 the core promoter of patients with a high replication status was less than that in those with a low replication status. Mutations were mainly distributed in basia core promoter (BCP) and the inbibitor region of Kunitz-type serine protease. This difference was not associated with mother or child. CONCLUSION: The different replication status of HBV is caused by mutations in the core promoter in mother and child infected hy mother-to-infant transmission and appears to be not associated with the status of development of the infection.OBJECTIVE: To study the relationship between the different replication status of hepatitis B virus (HBV) and mutations in the core promoter (CP) in mother and her child infected by mother-to-infant transmission. METHODS: The core promoter was amplified by PCR and cloned into pGEM-T vector with the T-A choning technique. The recombinant plasmid pGEM-CP was confirmed by digestion with restriction enzyme Apa I and Sac I. Two clones were selected to be sequenced in 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 the core promoter of patients with a high replication status was less than that in those with a low replication status. Mutations were mainly distributed in basia core promoter (BCP) and the inbibitor region of Kunitz-type serine protease. This difference was not associated with mother or child. CONCLUSION: The different replication status of HBV is caused by mutations in the core promoter in mother and child infected hy mother-to-infant transmission and appears to be not associated with the status of development of the infection.

关 键 词：HBV mother-to-infant transmission REPLICATION core promoter mutation 

分 类 号：R512.62[医药卫生—内科学] R725.1[医药卫生—临床医学]