Ngui S L, O'Connell S, Eglin R P, Heptonstall J, Teo C G
Virus Reference Division, Central Public Health Laboratory, Communicable Disease Surveillance Centre, London, United Kingdom.
J Infect Dis. 1997 Nov;176(5):1360-5. doi: 10.1086/514133.
Hepatitis B virus (HBV) infection occurred despite full passive-active immunoprophylaxis in 20 of 321 infants born to mothers seropositive for hepatitis B e antigen. In 2 (12%) of 17 infected infants, mother-infant DNA sequence mismatches were found in a segment of the HBV S gene coding for antigenic determinants of the HBV surface antigen (HBsAg) amplified from sera by polymerase chain reaction (PCR). Point substitutions occurred in codons 120, 134, and 144 of the HBsAg polypeptide in the variant sequence of 1 infant and in codon 126 in the other; all were missense mutations. Mutant sequences could not be recovered from maternal sera by PCR cloning but were selectively generated using an amplification refractory mutation system. The frequency of potential vaccine escape mutants is therefore low, and these preexist maternally as minor variants.
在321名母亲乙肝e抗原血清学阳性的婴儿中，有20名婴儿尽管接受了全程被动 - 主动免疫预防，仍发生了乙型肝炎病毒（HBV）感染。在17名受感染婴儿中的2名（12%）中，通过聚合酶链反应（PCR）从血清中扩增出编码HBV表面抗原（HBsAg）抗原决定簇的HBV S基因片段，发现母婴DNA序列不匹配。在1名婴儿的变异序列中，HBsAg多肽的第120、134和144密码子发生了点替换，另一名婴儿的第126密码子发生了点替换；所有这些都是错义突变。通过PCR克隆无法从母亲血清中回收突变序列，但使用扩增阻滞突变系统可选择性地产生突变序列。因此，潜在疫苗逃逸突变体的频率较低，并且这些突变体在母亲体内以次要变异体的形式预先存在。
