||Coseo S, Porras C, Hildesheim A, Rodriguez AC, Schiffman M, Herrero R, Wacholder S, Gonzalez P, Wang SS, Sherman ME, Jimenez S, Solomon D, Bougelet C, van Doorn LJ, Quint W, Safaeian M, Costa Rica HPV Vaccine Trial (CVT) Group, Alfaro M, Barrantes M, Bratti MC, Cárdenas F, Cortés B, Espinoza A, Estrada Y, Gonzalez P, Guillén D, Herrero R, Jimenez SE, Morales J, Morera LA, Pérez E, Porras C, Rodriguez AC, Villegas M, Freer E, Bonilla J, Silva S, Atmella I, Ramírez M, Macklin N, Hildesheim A, Lowy DR, Schiffman M, Schiller JT, Sherman M, Solomon D, Wacholder S, Pinto L, Garcia-Pineres A, Eklund C, Hutchinson M, Quint W, van Doorn LJ, Bougelet C
||BACKGROUND: Serological indicators of human papillomavirus (HPV) infection are being used to differentiate HPV-naïve from previously infected women in vaccine and epidemiologic/clinical studies. We investigated HPV16 and 18 seroepidemiology among young, unvaccinated women aged between 18 and 25. MATERIALS AND METHODS: We conducted a cross-sectional evaluation of the enrollment visit in the ongoing community-based HPV16/18 Costa Rica Vaccine Trial. Prevaccination serum immunoglobulin G (IgG) antibodies were measured against HPV16 and HPV18 by enzyme-linked immunosorbent assay; cervical samples were tested for HPV DNA using Hybrid Capture 2 and SPF10/LiPA25. Seroprevalence and its correlates were evaluated using unconditional logistic regression. RESULTS: Among 5871 nonvirginal women, HPV16 and 18 seroprevalences were 30.8% and 28.1%, HPV16 and HPV18 DNA prevalences were 8.3% and 3.2%, respectively. About 37% of HPV16 DNA-positives and 42% of HPV18 DNA-positives were seronegative. Seroprevalence increased with time since sexual debut, whereas DNA prevalence did not. The correlates of HPV16 and/or 18 seropositivity were related to sexual behaviors, particularly higher number of lifetime sexual partners. There was no evidence of assay cross-reactivity as HPV16 seroprevalence was similar (approximately 34%) among women singly infected with genetically and nongenetically related species (α9 and non-α9); likewise, seropositivity to HPV18 was similar (approximately 30%) among women singly infected with α7 and non-α7 species. CONCLUSIONS: The increasing seroprevalence observed with time since first sex suggests that HPV serology is a cumulative marker of HPV exposure. However, many DNA infected women were seronegative; thus, serology is an imperfect measure of past exposure to cervical HPV, at best. Additionally, we found no evidence of assay cross-reactivity.