© 2000 by Oxford University Press
Journal of the National Cancer Institute, Vol. 92, No. 6, 464-474,
March 15, 2000
© 2000 Oxford University Press
Population-Based Study of Human Papillomavirus Infection and Cervical Neoplasia in Rural Costa Rica
Affiliations of authors: R. Herrero (formerly at the Ministry of Health, San Jose, Costa Rica), M. Plummer, International Agency for Research on Cancer, Lyon, France; A. Hildesheim, S. Wacholder, M. Schiffman, Epidemiology and Biostatistics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD; C. Bratti, J. Morales, I. Balmaceda, M. Alfaro, Caja Costarricense de Seguro Social, San Jose, Costa Rica; M. E. Sherman, Epidemiology and Biostatistics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, and Department of Pathology and Gynecology and Obstetrics, The Johns Hopkins Medical Institutions, Baltimore, MD; M. Hutchinson, Women and Infants' Hospital, Brown University, Providence, RI; M. D. Greenberg, Omnia Corporation, Philadelphia, PA; R. D. Burk, Departments of Pediatrics, Microbiology and Immunology and Epidemiology and Social Medicine, Albert Einstein College of Medicine, Bronx, NY.
Correspondence to present address: Rolando Herrero, M.D., Ph.D., Proyecto Epidemiologico Guanacaste, P.O. Box 301-6151, San Jose, Costa Rica (e-mail: rherrero{at}amnet.co.cr).
BACKGROUND: Human papillomavirus (HPV) is the main cause of cervical neoplasia. Because few population-based studies have investigated the prevalence of type-specific infection in relation to cervical disease, we studied a high-risk population, estimating the prevalence of HPV infection and the risk associated with various HPV types. METHODS: We screened 9175 women in Guanacaste, Costa Rica, to obtain a referent standard final diagnosis, and tested 3024 women for more than 40 types of HPV with a polymerase chain reaction-based system. RESULTS: Among women with normal cytology, HPV infections peaked first in women younger than 25 years, and they peaked again at age 55 years or older with predominantly non-cancer-associated types of HPV and uncharacterized HPV types. Low-grade squamous intraepithelial lesions (LSILs) (n = 189) decreased consistently with age. The prevalence of high-grade squamous intraepithelial lesions (HSILs) (n = 128) peaked first around age 30 years and again at age 65 years or older. Seventy-three percent of LSILs were HPV positive, with HPV16 being the predominant type (16% of positive subjects). HPV was found in 89% of HSILs and 88% of cancers, with HPV16 being strongly predominant (51% and 53% of positive subjects). Virtually all HSILs and cancers had cancer-associated HPV types, with high odds ratios (ORs) and attributable fractions around 80%. Risk for HPV16 was particularly high (OR for HSILs = 320, 95% confidence interval [CI] = 97-1000; OR for cancer = 710, 95% CI = 110-4500). CONCLUSIONS: We confirm the early decline of HPV infection with age but note increased prevalence after menopause, which could be related to a second peak of HSILs, an observation that warrants further investigation. At least 80% of HPVs involved in cervical carcinogenesis in this population have been characterized. Polyvalent vaccines including the main cancer-associated HPV types may be able to prevent most cases of cervical disease in this region.
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