Patti E Gravitt1, Morgan Marks2, Margaret Kosek3, Christine Huang4, Lilia Cabrera5, Maribel Paredes Olortegui5, Alberto Mejia Medrano4, Dixner R Trigoso5, Sarah Qureshi6, Gustavo S Bardales7, Javier Manrique-Hinojosa7, Albert Z Cardenas7, Manuel A Larraondo7, Jaime Cok8, Fares Qeadan9, Mark Siracusa10, Robert H Gilman6. 1. Department of Pathology Department of Epidemiology. 2. Department of Epidemiology Department of Pharmacoepidemiology, Merck Research Laboratories, Whitehouse Station. 3. Department of International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland Biomedical Research Unit, Asociación Benéfica PRISMA. 4. Departamento de Ginecologia, Hospital Regional de Loreto, Iquitos. 5. Biomedical Research Unit, Asociación Benéfica PRISMA. 6. Department of International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. 7. Intituto de Enfermedades Neoplasicas. 8. Hospital Cayetano Heredia, Universidad Peruana Cayetano Heredia, Lima, Peru. 9. Department of Internal Medicine, University of New Mexico, Albuquerque. 10. Department of Medicine, New Jersey Medical School, Rutgers-The State University of New Jersey, Newark.
Abstract
BACKGROUND: An ecological correlation between invasive cervical cancer incidence and burden of soil-transmitted helminths (STH) is hypothesized to explain the excess in detectable human papillomavirus (HPV) infection in Latin America, via a global T-helper type 2 (Th2)-biased mucosal immune response secondary to STH infection. METHODS: The association between current STH infection and HPV prevalence was compared in regions of Peru where STH is or is not endemic. Adjusted prevalence ratios (PRs) with robust variance were estimated as an effect measure of STH infection on HPV prevalence in each study site. Soluble immune marker profiles in STH-infected and STH-uninfected women were compared using Spearman rank correlation with the Sidak correction. RESULTS: Among women in the helminth-endemic region of the Peruvian Amazon, those with STH infection women had a 60% higher prevalence of HPV, compared with those without STH infection (PR, 1.6; 95% confidence interval, 1.0-2.7). Non-STH parasitic/protozoal infections in the non-STH-endemic population of Peru were not associated with HPV prevalence. In Iquitos, A Th2 immune profile was observed in cervical fluid from helminth-infected women but not helminth-uninfected women. CONCLUSIONS: A proportion of the increased HPV prevalence at older ages observed in Latin America may be due to a population-level difference in the efficiency of immunological control of HPV across the lifespan due to endemic STH infection.
BACKGROUND: An ecological correlation between invasive cervical cancer incidence and burden of soil-transmitted helminths (STH) is hypothesized to explain the excess in detectable human papillomavirus (HPV) infection in Latin America, via a global T-helper type 2 (Th2)-biased mucosal immune response secondary to STH infection. METHODS: The association between current STH infection and HPV prevalence was compared in regions of Peru where STH is or is not endemic. Adjusted prevalence ratios (PRs) with robust variance were estimated as an effect measure of STH infection on HPV prevalence in each study site. Soluble immune marker profiles in STH-infected and STH-uninfected women were compared using Spearman rank correlation with the Sidak correction. RESULTS: Among women in the helminth-endemic region of the Peruvian Amazon, those with STH infection women had a 60% higher prevalence of HPV, compared with those without STH infection (PR, 1.6; 95% confidence interval, 1.0-2.7). Non-STH parasitic/protozoal infections in the non-STH-endemic population of Peru were not associated with HPV prevalence. In Iquitos, A Th2 immune profile was observed in cervical fluid from helminth-infected women but not helminth-uninfected women. CONCLUSIONS: A proportion of the increased HPV prevalence at older ages observed in Latin America may be due to a population-level difference in the efficiency of immunological control of HPV across the lifespan due to endemic STH infection.
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