Low Detection Rate and Maternal Provenance of Hepatitis B Virus S Gene Mutants in Cases of Failed Postnatal Immunoprophylaxis in England and Wales

• Published in: The Journal of infectious diseases 1997-11, Vol.176 (5), p.1360-1365
• Main Authors: Ngui, S. L., O'Connell, S., Eglin, R. P., Heptonstall, J., Teo, C. G.
• Format: Article
• Language: English
• Subjects: Amino Acid Sequence; Annealing; Biological and medical sciences; Codon; Codons; Concise Communications; Epidemiology; Female; Fundamental and applied biological sciences. Psychology; Genetic mutation; Hepatitis antigens; Hepatitis B - prevention & control; Hepatitis B Surface Antigens - genetics; Hepatitis B virus; Human viral diseases; Humans; Immunization, Passive; Immunoglobulins - immunology; Infant; Infant, Newborn; Infants; Infections; Infectious Disease Transmission, Vertical - prevention & control; Infectious diseases; Medical sciences; Microbiology; Molecular Sequence Data; Mutation; Polymerase Chain Reaction; Pregnancy; Public health; Vaccination; Viral diseases; Viral hepatitis; Virology
• ISSN: 0022-1899; 1537-6613
• 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.