| Abstrakt: |
High‐risk human papillomaviruses, such as type 16 (HPV‐16), are established etiological agents for cervical carcinoma. In most cases, this virus is transmitted sexually, though can also be spread from mother to infant at delivery. We have demonstrated previously a high prevalence (∼52%) of HPV‐16 DNA in the mouths of prepubertal children, albeit with low levels of transcription [Rice et al., 2000]. We investigated whether childhood buccal infections with HPV‐16 are persistent or transient and whether children became infected through contact with their immediate family members. Two groups of children were selected: one group were all initially HPV‐16 E5 DNA‐positive in sensitive polymerase chain reaction tests of swabs from their buccal mucosa (n = 20), and the other group consisted of children who were all HPV‐16 E5‐negative (n = 19). Thirty months later, a second oral swab was collected from each child and tested for HPV DNA. At this second visit, 40% of the HPV‐16‐positive group had no detectable HPV‐16 DNA; conversely, 63% of children who were originally HPV‐16‐negative had now acquired the virus. Three months later, a third sample was collected from eight children and their immediate families (seven were HPV‐16 E5 DNA‐positive at the second visit). Amongst the family samples tested, in two families a single previously untested child was HPV‐16 DNA‐positive. It is concluded that HPV‐16 DNA in the oral cavities of children is a transient event and is most probably acquired from their peers. J. Med. Virol. 71:593–598, 2003. © 2003 Wiley‐Liss, Inc. |
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