Epidemiology

British Journal of Cancer (2003) 89, 1248–1254. doi:10.1038/sj.bjc.6601272 www.bjcancer.com
Published online 30 September 2003

Seroprevalence of human papillomavirus-16, -18, -31, and -45 in a population-based cohort of 10 000 women in Costa Rica

Presented in part at the 20th International Papillomavirus Conference, Paris, France, October 2002, Abstract No. 071.

Written informed consent was obtained from all participants, in accordance with US Department of Health and Human Services guidelines. This study was approved by the institutional review boards at the NIH and in Costa Rica.

S S Wang1, M Schiffman1, T S Shields1, R Herrero2, A Hildesheim1, M C Bratti2, M E Sherman1, A C Rodriguez2, P E Castle1, J Morales2, M Alfaro2, T Wright3, S Chen4, B Clayman5, R D Burk6 and R P Viscidi5

  1. 1National Cancer Institute, Bethesda, MD 20892-7234, USA
  2. 2Proyecto Epidemiologico Guanacaste, FUCODOCSA, Costa Rica 1253-1007, Mexico
  3. 3College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
  4. 4Information Management Services, Inc., Silver Spring, MD 20904, USA
  5. 5Stanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
  6. 6Albert Einstein College of Medicine, Bronx, NY 10461, USA

Correspondence: Dr SS Wang, Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd., EPS MSC# 7234, Bethesda, MD 20892-7234, USA. E-mail: wangso@mail.nih.gov

Received 29 May 2003; Revised 18 July 2003; Accepted 23 July 2003.

Top

Abstract

Human papillomavirus (HPV) seroprevalence and determinants of seropositivity were assessed in a 10 049-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.

Keywords:

HPV, seroprevalence, cervical cancer, predictors