Evidence for HPV DNA in the placenta of women who resorted to elective abortion.

BACKGROUND: It is believed that HPV infection can result in the death of placental trophoblasts and cause miscarriages or preterm birth. In clinical cases of placental villi positive for HPV DNA reported by other authors, contamination is suspected in the act of crossing the cervical canal. We analyzed placental samples of women who resorted to elective abortion obtained by hysterosuction of ovular material, bypassing any contact with the cervical canal and vagina. METHODS: We studied the chorionic villi of the placenta of 64 women who resorted to voluntary termination of pregnancy, in the first trimester. To avoid contamination of the villi by the cervical canal, we analyzed placental samples obtained by hysterosuction of ovular material, bypassing any contact with the cervical canal and vagina. All samples of chorionic villi were manually selected from the aborted material and subjected to research for HPV DNA. RESULTS: HPV DNA was detected in 10 out of 60 women (16.6%). The HPV DNA identified in the placenta belonged to genotypes 6, 16, 35, 53, and 90. CONCLUSION: The study shows that papillomavirus DNA can infect the placenta and that placenta HPV infection can occur as early as the first trimester of pregnancy.

Progression of CIN1/LSIL HPV Persistent of the Cervix: Actual Progression or CIN3 Coexistence.

Objective: The natural history of the CIN1 lesions is characterized by an elevated rate of spontaneous regression (80%), some authors recognize a capacity to progress to HSIL in 10% of cases, and other authors do not recognize the capacity of progression of LSIL (CIN1). This study was aimed to evaluate the incidence of progression to HSIL (CIN3) in women with a histological diagnosis of LSIL (CIN1). Furthermore, to this end, we studied the histological outcomes of cone specimens collected by the LEEP. Methods: All the data were retrospectively analyzed. All participants underwent a follow-up of 4 years, during which each woman underwent an HPV test and genotyping, cervical cytological sampling, or biopsy every six months. The endpoint was the histological confirmation of CIN3 lesions in any moment during follow-up. Results: Progression to CIN3 occurred in 7 cases (1,5%). Analyzing the histological exams of the cones of the 7 cases that progressed to CIN3, we found the coexistence of CIN1 and CIN3 lesions in all cases. Conclusion: After 4 years of follow-up, only 1.5% (7/475) of the women with LSIL developed CIN3, all within the first two years of follow-up, and were immediately treated. The most likely explanations for "progression" from LSIL to HSIL are (1) actual progression, (2) underdiagnosis of HSIL on initial biopsy, (3) overdiagnosis of HSIL on follow-up biopsy/cone, and (4) CIN3 arose de novo. Analyzing the histological exams of the cones of the 7 cases that progressed to high-grade, we found the coexistence of CIN1 and CIN3 lesions in all cases. Some recent studies have shown that a viral genotype corresponds to different lesions in the same cervix; therefore, CIN1 coexisting with CIN3 does not always indicate progression of CIN1. Other authors have doubted the capacity of LSIL to progress.