This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Viscidi, R. P. Articles by Burk, R. D. Search for Related Content PubMed PubMed Citation Articles by Viscidi, R. P. Articles by Burk, R. D.

Seroreactivity to Human Papillomavirus (HPV) Types 16, 18, or 31 and Risk of Subsequent HPV Infection

Results from a Population-Based Study in Costa Rica

¹ Johns Hopkins University School of Medicine, Baltimore, Maryland; ² Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland; ³ Proyecto Epidemiológico Guanacaste, Costa Rican Foundation for Health Sciences, San José, Costa Rica; and ⁴ Albert Einstein College of Medicine, Bronx, New York

Whether antibodies to human papillomavirus (HPV) capsids, elicited by natural infection, are protective is unknown. This question was addressed in a population-based cohort of 7046 women in Costa Rica by examining the association between baseline seroreactivity to HPV-16, HPV-18, or HPV-31 virus-like particles and the risk of subsequent HPV infection at a follow-up visit 5–7 years after enrollment. Seropositivity to HPV-16, HPV-18, or HPV-31 was not associated with a statistically significant decreased risk of infection with the homologous HPV type [relative risk (RR) and [95% confidence interval (CI)], 0.74 (0.45–1.2), 1.5 (0.83–2.7), and 0.94 (0.48–1.8), respectively]. Seropositivity to HPV-16 or HPV-31 was not associated with a decreased risk of infection with HPV-16 or its genetically related types [RR (95% CI), 0.82 (0.61–1.1) and 0.93 (0.68–1.2), respectively]. Seropositivity to HPV-18 was not associated with a decreased risk of infection with HPV-18 or its genetically related types (RR 1.3; 95% CI 1.0–1.8). Thus, we did not observe immunity, although a protective effect from natural infection cannot be excluded because of the limits of available assays and study designs.

This article has been cited by other articles:

				M. J. J. Fleury, A. Touze, S. de Sanjose, F. X. Bosch, J. Klaustermeiyer, and P. Coursaget Detection of Human Papillomavirus Type 31-Neutralizing Antibodies from Naturally Infected Patients by an Assay Based on Intracellular Assembly of Luciferase-Expressing Pseudovirions Clin. Vaccine Immunol., January 1, 2008; 15(1): 172 - 175. [Abstract] [Full Text] [PDF]

				S. Dillon, T. Sasagawa, A. Crawford, J. Prestidge, M. K. Inder, J. Jerram, A. A. Mercer, and M. Hibma Resolution of cervical dysplasia is associated with T-cell proliferative responses to human papillomavirus type 16 E2 J. Gen. Virol., March 1, 2007; 88(3): 803 - 813. [Abstract] [Full Text] [PDF]

				M. J. Silverberg, M. F. Schneider, B. Silver, K. M. Anastos, R. D. Burk, H. Minkoff, J. Palefsky, A. M. Levine, and R. P. Viscidi Serological Detection of Human Papillomavirus Type 16 Infection in Human Immunodeficiency Virus (HIV)-Positive and High-Risk HIV-Negative Women Clin. Vaccine Immunol., April 1, 2006; 13(4): 511 - 519. [Abstract] [Full Text] [PDF]

				R. P. Viscidi, B. Snyder, S. Cu-Uvin, J. W. Hogan, B. Clayman, R. S. Klein, J. Sobel, and K. V. Shah Human Papillomavirus Capsid Antibody Response to Natural Infection and Risk of Subsequent HPV Infection in HIV-Positive and HIV-Negative Women Cancer Epidemiol. Biomarkers Prev., January 1, 2005; 14(1): 283 - 288. [Abstract] [Full Text] [PDF]