The Medline-indexed literature on risk factors for HPV infection and HPV transmission is critically reviewed. Principles for assay validation and interpretation, reliability of different study designs and principles for interpretation of conflicting reports are discussed. The conclusions arrived at
High risk genital papillomavirus infections are spread vertically
✍ Scribed by Philip S. Rice; John Cason; Jennifer M. Best; J. E. Banatvala
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 137 KB
- Volume
- 9
- Category
- Article
- ISSN
- 1052-9276
No coin nor oath required. For personal study only.
✦ Synopsis
It is well recognised that high-risk human papillomaviruses (HPVs) are spread by sexual activity, but the possibility of non-sexual transmission remains controversial. We present evidence for vertical transmission from at least 30% HPV positive mothers to their infants, resulting in persistent infection in children. That the mother is the source of infant infection has been confirmed by DNA sequencing. We also discuss the evidence for oral HPV-16 infection in children. In our own studies, HPV-16 DNA was detected in buccal cells from 48% children, aged 3-11 and transcriptionally active infection was confirmed in some children. Other studies have reported prevalences of 19%-27% among children less than 11 years of age. Studies that have failed to detect high-risk HPVs in children have used techniques which were insufficiently sensitive to detect the low levels of virus present. Serological studies also suggest that c45% prepubertal children have acquired HPV-16. Thus, convincing evidence is now available for vertical transmission of high risk HPVs, which probably results in widespread infection among children. The consequences of such infections remain to be elucidated.
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