Human papillomavirus infections in children: the potential role of maternal transmission.
To date, more than 100 types of human papillomavirus (HPV) have been identified. In the past 20 years, there has been an increasing interest in HPVs because of their potential role in the pathogenesis of malignant tumors. HPV infections are known to affect predominantly adult, sexually active age groups, whereas skin warts, at various anatomic sites, are usually associated with younger individuals. The modes of viral transmission in children remain controversial, including perinatal transmission, auto- and hetero-inoculation, sexual abuse, and, possibly, indirect transmission via fomites. Recent studies on perinatal infection with HPV have been inconclusive. It is still unclear how frequently perinatal infection progresses to clinical lesions, whether genital, laryngeal, or oral. Conflicting reports have been published on the prevalence of HPV infections in children. The current consensus is, however, that newborn babies can be exposed to cervical HPV infection of the mother. The detection rate of HPV DNA in oral swabs of newborn babies varies from 4% to 87%. The concordance of HPV types detected in newborn babies and their mothers is in the range of 57% to 69%, indicating that the infants might acquire the HPV infection post-natally from a variety of sources. HPV antibodies have been detected in 10% to 57% of the children, and there is usually no correlation between seropositivity and the detection of HPV DNA in either the oral or the genital mucosa. There is also evidence that transmission in utero or post-natal acquisition is possible. The mode of in utero transmission remains unknown, but theoretically the virus could be acquired hematogenously, by semen at fertilization, or as an ascending infection in the mother. The understanding of viral transmission routes is important, particularly because several vaccination programs are being planned worldwide. The serologic response to HPV detected in different populations of young women or women at risk of cervical cancer might be due to genital infections, but the possibility that HPV infection has been acquired earlier in life through the oral mucosa or respiratory tract cannot be ruled out.
Syrjänen
S
S
Department of Oral Pathology and Radiology, Institute of Dentistry, Turku, Finland. stina.syrjanen@utu.fi
Puranen
M
M
D000328:Adult; D000914:Antibodies, Viral / Q000032:analysis; D002648:Child; D002650:Child Abuse, Sexual; D003218:Condylomata Acuminata / Q000821:virology; D004279:DNA, Viral / Q000032:analysis; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D018445:Infectious Disease Transmission, Vertical; D007822:Laryngeal Neoplasms / Q000821:virology; D009055:Mouth / Q000821:virology; D009059:Mouth Diseases / Q000821:virology; D010212:Papilloma / Q000821:virology; D027383:Papillomaviridae / Q000145:classification / Q000235:genetics / Q000276:immunology; D030361:Papillomavirus Infections / Q000151:congenital / Q000517:prevention & control / Q000635:transmission*; D011247:Pregnancy; D012307:Risk Factors; D014412:Tumor Virus Infections / Q000151:congenital / Q000517:prevention & control / Q000635:transmission*; D002577:Uterine Cervical Diseases / Q000821:virology; D002583:Uterine Cervical Neoplasms / Q000821:virology; D014611:Vaccination; D014765:Viral Vaccines
D000914:Antibodies, Viral; D004279:DNA, Viral; D014765:Viral Vaccines