Human Papillomavirus Infections in Children: the Potential Role of Maternal Transmission

Abstract

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.

Human papillomavirus type 16 in head and neck carcinogenesis

“…It is unknown how these children originally acquired the HPV-16 DNA in their tonsils. Vertical transmission of HPV from mothers to their children, or additional sources such as breast milk, siblings via kissing, or exposure to contaminated fomites is feasible, as suggested in one review (Syrjänen and Puranen 2000). In our study population, no patients older than 33 years was positive for HPV DNA in their tonsils, allowing speculation that, if these patients did not develop precancer or cancer lesions, HPV-16 DNA had been cleared by their immune system.…”

Distinct regulation and impact of type 1 T‐cell immunity against HPV16 L1, E2 and E6 antigens during HPV16‐induced cervical infection and neoplasia

“…Interestingly, the most immunodominant region of HPV16 L1 that is recognized by healthy subjects in our study is located outside this area and shows predominantly homology with HPV types that are members of the HPV-clade A9 (types 16, 31, 33, 35, 52, 58; Table IV). The total absence of detectable HPV16 L1 peptide-specific T-cell immunity in the group of young virgin female subjects 10-15 years of age, who will have encountered most of the low-risk and skin types of HPV, [37][38][39][40][41][42][43] further indicates that cross-reactivity at the T-cell level does not readily occur between these common HPV types and the high-risk HPV types. The high conservation of HPV16 L1 within the HPV types of clade A9 suggests that L1-specific T-cell cross-reactivity against these group members could occur.…”

“…[38][39][40][41][42][43] The small amounts of blood available from these children necessitated the use of 3 large pools of HPV16 L1 peptides, covering amino acids 1-180, 166-345 and 331-505. The use of pools of 11 peptides will result in some loss of specificity with respect to the exact sequences recognized.…”

Çocukluk Çağında Anogenıtal Verru ve Cinsel İstismar

“…DNA'ları çift sarmal yapıda, yaklaşık 8000 baz çifti içeren ve zarfsız olduğu için kuru, ısı, donma ve çeşitli kimyasal maddelerle inaktivasyona direnç gösteren bir virüstür (4,5). Çocuklarda klinik hastalıklara neden olan 200'den fazla tipi bulunmaktadır (6,7). HPV tiplerinin farklı biyolojik, moleküler ve kimyasal özelliklere sahip bulunması, bu genomik çeşitliliğin HPV patojenitesinde ve doğal seyrinde de farklı görünümlere sahip olmasına yol açmıştır (8).…”

“…Vertikal bulaş, yenidoğanın doğum kanalından inişi sırasında kontaminasyonla veya in utero hayatta virüsün membranlardan geçişi veya kan yoluyla transplesantal geçiş şeklinde meydana gelebilmektedir (6). Yapılan bir çalışmada periferal kan mononükleer hücrelerde HPV16 DNA bulunan 7 annenin bebeklerinin kord kanlarında da aynı DNA'nın olduğu gösterilmiştir (20).…”