PreS/S gene mutations in HBV in children infected through mother-to-infant transmission and in their mothers / 中华肝脏病杂志

ABSTRACT

<p><b>OBJECTIVES</b>To investigate the characteristics of mutations in PreS/S gene of HBV in children infected through mother-to-infant transmission and in their mothers with different degree of viremia.</p><p><b>METHODS</b>There were 15 pairs of child and mother in this study. Mothers of all children were chronic asymptomatic HBsAg carrier (ASC) before pregnancy and the children were not inoculated against HBV after birth. Anti-HBV medicine was never administrated to all subjects. The serological markers of hepatitis A, B, C, D and E virus were tested and the titers of serum HBV DNA were quantitated. PreS/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. Two clones were selected to be sequenced from each patient.</p><p><b>RESULTS</b>According to the degree of viremia in every pair of mother and child, 15 pairs of child and mother were divided into three groups group A (both children and mothers had high viremia with HBeAg-positive), group B (high in children and low in mothers with anti-HBe positive), and group C (low in children and high in mothers), and there were 5 pairs in each group. The subtype of each pair was the same. There were 4/5 pairs of HBV with B/adw2 and 1/5 pair of HBV with C/adrq+ in each group. It was shown that there were no difference among the four high viremia groups or between the two low viremia groups in the number of mutations and the number of mutational positions. However, there was significant difference between high viremia group and low viremia group. The mutation was not related to age. There were 56 mutational positions and there was no mutational hotspot in high viremia patients. In two low viremia groups (the mothers in group B and the children in group C), there were 113 mutational positions and 85 mutational positions were hotspots (owned by 5/8 clones in each) which could make 37 amino acids changed. Most of mutational amino acids were located within T and B cell epitopes of envelope protein or/and located in the surrounding regions.</p><p><b>CONCLUSIONS</b>There are many differences in HBV with different degree of viremia, even if it comes from the same strain. There are some regular patterns in the mutations of HBV after HBeAg seroconversion happened.</p>