Transplacental transmission of Human Papillomavirus

Placenta Human papillomavirus (HPV), the most common sexually transmitted infection, has been recognized as a cause of anogenital warts (HPV type 6 and 11) and cervical cancer (HPV type 16, 18 and others). In children, HPV-related (type 6 and 11) laryngeal papillomas, conjunctival papillomas and genital warts. Although it has been established that HPV is sexually transmitted, there is growing evidence that non-sexual transmission also occurs. This includes vertical transmission from parents to infants, horizontal transmission from other family members and those in close contact with the child, autoinoculation from one site to another and possibly indirect transmission via phomites. The potential mother-to-child HPV transmission route in the perinatal period has been demonstrated. There is evidence of vertical transmission, presumably occurring during passage of the fetus through an infected birth canal. The virus could also be transmitted by ascending infection, especially after premature rupture of the membranes. In utero transmission could be caused either by ascending infection from an infected birth canal, by sperm at fertilization or hematogenously (transplacentally). HPV DNA has been detected in peripheral blood mononuclear cells of pregnant women, cord blood specimens of neonates, oropharyngeal secretions of neonates, amniotic fluid, fetal membranes, placental trophoblastic cells, infants born by elective cesarean section delivery, and in syncytiotrophoblastic cells of spontaneously aborted material. In addition, there are type-discordant cases between mothers and newborns, suggesting that many of these infants did not acquire the HPV from their mothers. These observations could explain the transplacental transmission of HPV from an infected mother to the fetus. However, only a limited number of women have been studied to confirm placental transmission of HPV.

Transplacental transmission of Human Papillomavirus. Virology Journal 5: 106, 25 September 2008
This paper aimed at studying the transplacental transmission of HPV and looking at the epidemiological factors involved in maternal viral infection. The following sampling methods were used: (1) in the pregnant woman, (a) genital; (b) peripheral blood; (2) in the newborn, (a) oral cavity, axillary and inguinal regions; (b) nasopharyngeal aspirate, and (c) cord blood; (3) in the placenta. The HPV DNA was identified using two methods: multiplex PCR of human beta-globin and of HPV using the PGMY09 and PGMY11 primers; and nested-PCR, which combines degenerated primers of the E6/E7 regions of the HPV virus, that allowed the identification of genotypes 6/11, 16, 18, 31, 33, 42, 52 and 58. Transplacental transmission was considered when type-specific HPV concordance was found between the mother, the placenta and the newborn or the mother and cord blood. The study included 49 HPV DNA-positive pregnant women at delivery. Twelve placentas (24.5%, n=12/49) had a positive result for HPV DNA. Eleven newborn were HPV DNA positive in samples from the nasopharyngeal or buccal and body or cord blood. In 5 cases (10.2%, n=5/49) there was HPV type-specific agreement between genital/placenta/newborn samples. In one case (2%, n=1/49) there was type specific HPV concordance between genital/cord blood and also suggested transplacental transmission. A positive and significant correlation was observed between transplacental transmission of HPV infection and the maternal variables of immunodepression (HIV, p=0.011). In conclusion the study suggests placental infection in 23.3% of the cases studied and transplacental transmission in 12.2%. It is suggested that in future HPV DNA be researched in the normal endometrium of women of reproductive age. The possible consequence of fetal exposure to HPV should be observed.

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