Perinatal transmission of genital human papillomaviruses (HPVs), including HPV-16 and -18 which are associated with anogenital carcinomas have 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 persists 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 infants 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 cases, 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 proteins were expressed in insect cells via recombinant baculoviruses and sera from 229 children were examined to determine at what age IgM antibodies 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 observation that infection with high cancer risk genital HPVs may occur in early life and persist is of considerable importance for HPV vaccine strategies.

Whilst genital papillomaviruses are commonly believed to be sexually transmitted, transmission of human papillomavirus type 16 (HPV-16) from mother to child at delivery has been described previously [Pakarian et al. (in press) British Journal of Obstetrics and Gynaecology]. In order to determine whether viral load in cervical/vaginal cells was an important determinant of transmission 15 pregnant women with HPV-16 infections were studied. Eight of these women had infants who were positive for HPV-16 DNA at genital and/or buccal sites. Viral load was estimated by laser densitometry of polymerase chain reaction (PCR) products. The eight mothers--four with a previous history of abnormal smears and two with previous genital warts--who transmitted infection to their infants had significantly higher viral loads (P < 0.05) than those who did not. It is concluded that viral load is an important, but not the sole, determinant for the transmission of HPV-16 from mother to infant.

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