[A study of the characteristics of pre S/S gene mutation of hepatitis B virus (HBV) in mothers and HBV-infected children via mother-to-infant transmission].

OBJECTIVE

To investigate the characteristics of mutations in pre S/S gene of HBV in asymptomatic carrier (AsC) children infected through mother-to-infant transmission and their AsC mothers with different degree of viremia.

METHODS

According to the levels of viremia in every pair of mother and child, 15 pairs of child and mother were divided into three groups 5 pairs in each group in this study: group I (both children and mothers had high viremia), group II (children had high and mothers had low viremia) and group III (children had low and mothers had high viremia). pre S/S gene 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 ApaI and SacI. Tow clones were selected to be sequenced in each patient. The mutations of preS/S were compared with HBV DNA consensus sequence of Chongqing.

RESULTS

In each group the subtypes of HBV were B/adw2 in 4 pairs and C/adrq+ in one pair. The preS/S clones in patients infected with subtype B/adw2 HBV were analyzed. It was shown that there was no difference among the four high viremic groups or between the two low viremic groups in the number of mutation and the mutational position. However, there was significant difference between the high viremic group and low viremic group. The mutation was not related to age. In the two low viremic groups (the mothers of group II and the children of group III), there were 86-94 mutational positions in 13/16 clones. There were 86 same mutational positions causing 37 amino acid changes in 11/13 clones and 90 same mutational positions causing 38 amino acid changes in 2/13 clones. Most of the changed amino acids were located within T and B cell epitopes of the envelope protein or/and the surrounding regions. Sixty-two mutational positions that resulted in 28 amino acid changes were same in these two mutational sequences.

CONCLUSIONS

The mutation of HBV is not associated with the duration of infection. There are many differences of mutation when HBV comes from a same strain in hosts with different degrees of viremia. There are some regular patterns in the mutation of HBV after occurrence of HBeAg seroconversion. The mutation could be related to the escape of the attack of host's immunity.