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Comparative Study
. 2003 Oct 6;89(7):1248-54.
doi: 10.1038/sj.bjc.6601272.

Seroprevalence of human papillomavirus-16, -18, -31, and -45 in a population-based cohort of 10000 women in Costa Rica

S S Wang  1 , M Schiffman, T S Shields, R Herrero, A Hildesheim, M C Bratti, M E Sherman, A C Rodriguez, P E Castle, J Morales, M Alfaro, T Wright, S Chen, B Clayman, R D Burk, R P Viscidi
Affiliations
Comparative Study

Seroprevalence of human papillomavirus-16, -18, -31, and -45 in a population-based cohort of 10000 women in Costa Rica

S S Wang et al. Br J Cancer. .

Abstract

Human papillomavirus (HPV) seroprevalence and determinants of seropositivity were assessed in a 10049-woman population-based cohort in Guanacaste, Costa Rica. Serologic responses based on VLP-based ELISA were obtained from the plasma collected at study enrollment in 1993/1994 for HPV-16 (n=9949), HPV-18 (n=9928), HPV-31 (n=9932), and HPV-45 (n=3019). Seropositivity was defined as five standard deviations above the mean optical density obtained for studied virgins (n=573). HPV-16, -18, -31, and -45 seroprevalence was 15, 15, 16, and 11%, respectively. Of women DNA-positive for HPV-16, -18, -31, or -45, seropositivity was 45, 34, 51, and 28%, respectively. Peak HPV seroprevalence occurred a decade after DNA prevalence; lifetime number of sexual partners was the key determinant of seropositivity independent of DNA status and age. DNA- and sero-positive women showed the highest risk for concurrent CIN3/cancer, followed by DNA-positive, sero-negative women.

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Figures

Figure 1
Figure 1
Age distribution of HPV-16, -18, -31, and -45 seroprevalence* and DNA-prevalence** in Guanacaste, Costa Rica women. *Population-based HPV-16, -18, -31, and -45 serology prevalence is shown in black lines and includes study virgins. Black dotted lines denote seroprevalence excluding study virgins. **HPV DNA prevalence does not include study virgins.
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