Sl. Ngui et al., LOW DETECTION RATE AND MATERNAL PROVENANCE OF HEPATITIS-B VIRUS S-GENE MUTANTS IN CASES OF FAILED POSTNATAL IMMUNOPROPHYLAXIS IN ENGLAND AND WALES, The Journal of infectious diseases, 176(5), 1997, pp. 1360-1365
Hepatitis B virus (HBV) infection occurred despite full passive-active
immunoprophylaxis in 20 of 321 infants born to mothers seropositive f
or hepatitis B e antigen. In 2 (12%) of 17 infected infants, mother-in
fant 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 substitu
tions 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 w
ere missense mutations. Mutant sequences could not be recovered from m
aternal sera by PCR cloning but were selectively generated using an am
plification refractory mutation system, The frequency of potential vac
cine escape mutants is therefore low, and these preexist maternally as
minor variants.