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|Title:||Population-level impact, herd immunity and elimination after HPV vaccination: a systematic review and meta-analysis of predictions of 16 transmission-dynamic models.|
|Authors:||Brisson M; Bénard E; Drolet M; Bogaards JA; Baussano I; Vanska S; Jit M; Boily MC; Smith MA; Berkhof J; Canfell K; Chesson HW; Burger EA; Choi YH; De Blasio BF; De Vlas SJ; Guzzetta G; Hontelez JAC; Jepsen MR; Kim JJ; Lazzarato F; Mattijsse SM; Mikolajczyk R; Pavelyev A; Pillsbury M; Shafer LA; Tully SP; Turner HC; Usher C; Walsh C|
|Categories:||Cancer Control, Survivorship, and Outcomes Research - Resources and Infrastructure|
Cancer Type - Cervical Cancer
|Journal Title:||The Lancet Public Health|
|Page number start:||8|
|Page number end:||17|
|Abstract:||Background Modelling studies have been widely used to inform human papillomavirus (HPV) vaccination policy decisions; however, many models exist and it is not known whether they produce consistent predictions of population-level effectiveness and herd effects. We did a systematic review and meta-analysis of model predictions of the long-term population-level effectiveness of vaccination against HPV 16, 18, 6, and 11 infection in women and men, to examine the variability in predicted herd effects, incremental benefit of vaccinating boys, and potential for HPV-vaccine-type elimination. Methods We searched MEDLINE and Embase for transmission-dynamic modelling studies published between Jan 1, 2009, and April 28, 2015, that predicted the population-level impact of vaccination on HPV 6, 11, 16, and 18 infections in high-income countries. We contacted authors to determine whether they were willing to produce new predictions for standardised scenarios. Strategies investigated were girls-only vaccination and girls and boys vaccination at age 12 years. Base-case vaccine characteristics were 100% efficacy and lifetime protection. We did sensitivity analyses by varying vaccination coverage, vaccine efficacy, and duration of protection. For all scenarios we pooled model predictions of relative reductions in HPV prevalence (RRprev) over time after vaccination and summarised results using the median and 10th and 90th percentiles (80% uncertainty intervals [UI]). Findings 16 of 19 eligible models from ten high-income countries provided predictions. Under base-case assumptions, 40% vaccination coverage and girls-only vaccination, the RRprev of HPV 16 among women and men was 0·53 (80% UI 0·46–0·68) and 0·36 (0·28–0·61), respectively, after 70 years. With 80% girls-only vaccination coverage, the RRprev of HPV 16 among women and men was 0·93 (0·90–1·00) and 0·83 (0·75–1·00), respectively. Vaccinating boys in addition to girls increased the RRprev of HPV 16 among women and men by 0·18 (0·13–0·32) and 0·35 (0·27–0·39) for 40% coverage, and 0·07 (0·00–0·10) and 0·16 (0·01–0·25) for 80% coverage, respectively. The RRprev were greater for HPV 6, 11, and 18 than for HPV 16 for all scenarios investigated. Finally at 80% coverage, most models predicted that girls and boys vaccination would eliminate HPV 6, 11, 16, and 18, with a median RRprev of 1·00 for women and men for all four HPV types. Variability in pooled findings was low, but increased with lower vaccination coverage and shorter vaccine protection (from lifetime to 20 years). Interpretation Although HPV models differ in structure, data used for calibration, and settings, our population-level predictions were generally concordant and suggest that strong herd effects are expected from vaccinating girls only, even with coverage as low as 20%. Elimination of HPV 16, 18, 6, and 11 is possible if 80% coverage in girls and boys is reached and if high vaccine efficacy is maintained over time.|
|Division:||Cancer Research Division|
|Funding Body:||Canadian Institutes of Health Research.|
The main funder of this study was the Canadian Institutes of Health Research. We received support from the Canada Research Chairs programme (support for MB), an operating grant from the Canadian Institutes of Health Research (number MOP-119427), and a foundation scheme grant from the Canadian Institutes of Health Research (number FDN-143283). IB is supported by the European Community’s Seventh Framework Programme (FP7-HEALTH-2013; grant number 603019) and the Bill & Melinda Gates Foundation (number OPP1053353), and is an Honorary Research Fellow at the School of Public Health, Imperial College, London, UK. MRJ was supported by the National Institute for Health Research Health Protection Research Unit (NIHR HPRU) in Immunisation at the London School of Hygiene & Tropical Medicine in partnership with Public Health England. JB is supported from the European Community’s Seventh Framework Programme (FP7-HEALTH-2013; grant no. 603019). JJK and EAB are supported by the US National Cancer Institute of the National Institutes of Health (number R01CA160744). KC is supported by a NHMRC Career Development Fellowship Grant (number AP1082989).
|Appears in Collections:||Research Articles|
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