PERINATAL INFECTION AND PERSISTENCE OF HUMAN PAPILLOMAVIRUS TYPE-16 AND TYPE-18 IN INFANTS

Perinatal transmission of genital human papillomaviruses (HPVs), inclu ding HPV-16 and -18 which are associated with anogenital carcinomas ha ve been described previously [Pakarian et al. (1994): British Journal of Obstetrics and Gynaecology 101:514-517; Kaye et al. (1994) Journal of Medical Virology 44:415-421]. A study was undertaken to investigate whether HPV-16 and -18 DNA in infants contaminated at delivery persis ts until they are 6 months of age. Of 61 pregnant women recruited, 42 (68.8%) were HPV-16 and 13 (21.3%) were HPV-18 DNA positive. At 24 hr there were transmission rates from HPV DNA positive mothers to their i nfants of about 73% (HPV-16: 69%; HPV-18: 76.9%). Ten mothers who were both HPV-16 and -18 DNA positive produced six (60%) infants who were also doubly positive at 24 hr. HPV DNA persisted to 6 weeks in 79.5% ( HPV-16: 84%; HPV-18: 75%) of those infants who were positive at birth. At 6 months of age, persistent HPV-16 DNA was detected in 83.3% of ca ses, but HPV-18 DNA persistence at this time was 20%. To extend these observations over a greater age range of children HPV-16 L1 and L2 pro teins were expressed in insect cells via recombinant baculoviruses and sera from 229 children were examined to determine at what age IgM ant ibodies to HPV were acquired. There was a bimodal distribution of IgM seropositivity which peaked between 2 and 5 and 13 and 16 years of age , suggesting that two distinct modes of transmission may occur. The ob servation that infection with high cancer risk genital HPVs may occur in early life and persist is of considerable importance for HPV vaccin e strategies. (C) 1995 Wiley-Liss, Inc.