Terazawa S, Kojima M, Yamanaka T, Yotsumoto S, Okamoto H, Tsuda F, Miyakawa Y, Mayumi M
Department of Pediatrics, Prefectural Gero Hospital, Gifu-Ken, Japan.
Pediatr Res. 1991 Jan;29(1):5-9. doi: 10.1203/00006450-199101000-00002.
Clones of hepatitis B virus (HBV) DNA were propagated from sera of two babies who developed neonatal fulminant hepatitis B, as well as from sera of their mothers who carried HBV with antibody to hepatitis B e antigen, and the precore-region sequences were determined. A point mutation from guanine to adenine, converting codon 28 for tryptophan (TGG) to a stop codon (TAG), was detected in 18 of 20 HBV DNA clones from mother and all 31 clones from baby in one family, and invariably in 55 clones from mother and three clones from baby in the other family. These results indicate that HBV mutants defective in the precore region in some carrier mothers with antibody to hepatitis B e antigen may transmit fulminant hepatitis B to their babies.
从两名患新生儿暴发性乙型肝炎的婴儿血清以及携带乙肝病毒且有乙肝e抗原抗体的母亲血清中扩增出乙肝病毒（HBV）DNA克隆，并测定了前核心区序列。在一个家庭中，20个来自母亲的HBV DNA克隆中有18个以及来自婴儿的所有31个克隆中，检测到一个从鸟嘌呤到腺嘌呤的点突变，该突变将色氨酸密码子28（TGG）转换为终止密码子（TAG）；在另一个家庭中，55个来自母亲的克隆以及3个来自婴儿的克隆中均无一例外地检测到该突变。这些结果表明，一些携带乙肝e抗原抗体的携带者母亲体内存在前核心区缺陷的HBV突变体，可能会将暴发性乙型肝炎传染给她们的婴儿。
