OBJECTIVETo 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.

METHODSCore 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.

RESULTSEvery pair of mother and child had same serotype and genotype and the homology of nucleotides encoding "a" determinant was 98 to 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.

CONCLUSIONSThe 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.