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Perinatal infection and persistence of human papillomavirus types 16 and 18 in infants

J Cason1, J N Kaye, R J Jewers

  • 1Richard Dimbleby Laboratory of Cancer Virology, Department of Virology, Rayne Institute, London, United Kingdom.

Insights

Perinatal transmission of high-risk human papillomaviruses (HPVs) like HPV-16 and HPV-18 can occur, with DNA persisting in infants for months. This early-life infection is crucial for developing effective HPV vaccine strategies.

Area of Science:

  • Virology
  • Immunology
  • Public Health

Background:

  • Perinatal transmission of genital human papillomaviruses (HPVs), including high-risk types HPV-16 and HPV-18, has been previously documented.
  • These HPV types are significant risk factors for developing anogenital carcinomas.

Purpose of the Study:

  • To investigate the persistence of HPV-16 and HPV-18 DNA in infants up to six months of age after perinatal exposure.
  • To determine the age of acquisition of IgM antibodies to HPV in children, suggesting potential transmission modes.

Main Methods:

  • Recruitment of 61 pregnant women to assess HPV DNA presence in mothers and infants at birth, 24 hours, 6 weeks, and 6 months.
  • Expression of HPV-16 L1 and L2 proteins in insect cells using recombinant baculoviruses.
  • Examination of sera from 229 children for IgM antibodies to HPV to identify age of acquisition.

Main Results:

  • High transmission rates of HPV-16 (69%) and HPV-18 (76.9%) from mothers to infants at 24 hours postpartum.
  • Sustained HPV DNA persistence at 6 weeks (79.5%) and 6 months (HPV-16: 83.3%, HPV-18: 20%) in infected infants.
  • Bimodal distribution of IgM seropositivity in children, peaking between 2-5 and 13-16 years, indicating potential dual transmission routes.

Conclusions:

  • Early-life infection with high-risk genital HPVs is possible and can persist beyond infancy.
  • The findings have significant implications for the timing and strategy of HPV vaccination programs.
  • The observed bimodal antibody response suggests distinct pathways for HPV acquisition in childhood.

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