Joseph E Tota1, Agnihotram V Ramanakumar2, Luisa L Villa3, Harriet Richardson4, Ann N Burchell5, François Coutlée6, Eduardo L Franco7. 1. Division of Cancer Epidemiology, Department of Oncology Department of Epidemiology, Biostatistics, and Occupational Health, McGill University Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland. 2. Division of Cancer Epidemiology, Department of Oncology. 3. Department of Radiology and Oncology, School of Medicine, Universidade de São Paulo, Brazil. 4. Department of Community Health and Epidemiology, Queens University, Kingston. 5. Division of Cancer Epidemiology, Department of Oncology Department of Family and Community Medicine, St. Michael's Hospital Centre for Research on Inner City Health, Li Ka Shing Knowledge Institute, Toronto, Canada. 6. Département de Microbiologie et Infectiologie, Université de Montréal. 7. Division of Cancer Epidemiology, Department of Oncology Department of Epidemiology, Biostatistics, and Occupational Health, McGill University.
Abstract
BACKGROUND: Recent birth cohorts vaccinated against human papillomavirus (HPV) may be protected against up to 4 genotypes (HPV-6, -11, -16, and -18). If natural competition exists between these and other HPV types, then the prevalence of other types may increase after vaccination. METHODS: Cohort information from 3 studies was used to compare acquisition and clearance of 30 different HPV types (individually and grouped by species), according to infection status with vaccine-targeted types at baseline and the time of the index infection, respectively. Hazard ratios (HRs) were adjusted for predictors of multiple-type infection. RESULTS: Among 3200 females across all studies, 857 were infected with HPV at baseline, and 994 acquired new infections during follow-up. Females infected with HPV-16 were at higher risk of acquiring other α-9 HPV types (HR, 1.9; 95% confidence interval [CI], 1.2-3.0) but at similar risk of clearing existing α-9 HPV infections (HR, 0.9; 95% CI, .7-1.3). Females infected with vaccine-targeted types were generally at higher risk of acquiring additional types (HRs, > 1.0) and at equal risk of clearing existing infections. Accounting for multiple comparisons, none of the HRs of < 1.0 or >1.0 were statistically significant in our analyses of acquisition or clearance. CONCLUSIONS: Vaccine-targeted HPV types do not appear to compete with other types, suggesting that HPV type replacement is unlikely to occur.
BACKGROUND: Recent birth cohorts vaccinated against human papillomavirus (HPV) may be protected against up to 4 genotypes (HPV-6, -11, -16, and -18). If natural competition exists between these and other HPV types, then the prevalence of other types may increase after vaccination. METHODS: Cohort information from 3 studies was used to compare acquisition and clearance of 30 different HPV types (individually and grouped by species), according to infection status with vaccine-targeted types at baseline and the time of the index infection, respectively. Hazard ratios (HRs) were adjusted for predictors of multiple-type infection. RESULTS: Among 3200 females across all studies, 857 were infected with HPV at baseline, and 994 acquired new infections during follow-up. Females infected with HPV-16 were at higher risk of acquiring other α-9 HPV types (HR, 1.9; 95% confidence interval [CI], 1.2-3.0) but at similar risk of clearing existing α-9 HPV infections (HR, 0.9; 95% CI, .7-1.3). Females infected with vaccine-targeted types were generally at higher risk of acquiring additional types (HRs, > 1.0) and at equal risk of clearing existing infections. Accounting for multiple comparisons, none of the HRs of < 1.0 or >1.0 were statistically significant in our analyses of acquisition or clearance. CONCLUSIONS: Vaccine-targeted HPV types do not appear to compete with other types, suggesting that HPV type replacement is unlikely to occur.
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