Matthijsse Suzette M, Hontelez Jan A C, Naber Steffie K, van Rosmalen Joost, Rozemeijer Kirsten, Penning Corine, Bakker Roel, van Ballegooijen Marjolein, de Kok Inge M C M, de Vlas Sake J
Department of Public Health, Erasmus MC, University Medical Center Rotterdam, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands.
Department of Public Health, Erasmus MC, University Medical Center Rotterdam, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands.
Vaccine. 2015 Oct 5;33(41):5357-5364. doi: 10.1016/j.vaccine.2015.08.079. Epub 2015 Sep 5.
Mathematical modelling is used to estimate the effectiveness of HPV vaccination. These estimates depend strongly on herd immunity and thus on naturally acquired immunity, a mechanism of which little is known. We estimated the impact of different vaccination strategies on HPV-16 and HPV-18 transmission and cervical cancer incidence in the Netherlands, considering different acquired immunity mechanisms.
We used the STDSIM microsimulation model, and considered two mechanisms for acquired immunity after infection: (I) full immunity with variable duration; (II) cumulatively decreasing susceptibility to reinfection. Girls aged 13-16 years received vaccination (94.7% efficacy for HPV-16 and 92.3% for HPV-18) during a once-off catch-up campaign with 50% coverage, followed by annual vaccination of 12-year-old girls (60% coverage). Alternative vaccination scenarios included increased coverage, including boys, and lower vaccine efficacy.
HPV-16 incidence reduced by 64% under mechanism I and 75% under mechanism II; HPV-18 incidence reduced by 58% and 73%, respectively, and these reductions lead to 48-56% fewer cervical cancer cases. Increasing coverage can lead to over 96% reduction in HPV incidence. Vaccinating boys reduced incidence by 79-89% for HPV-16 and 83-98% for HPV-18 in women.
Effectiveness estimates of HPV vaccination differ slightly between different acquired immunity mechanisms, yet these differences are unlikely to affect policy decisions. Offering vaccination to boys as well may be considered to further reduce cancer incidence.
数学模型用于评估人乳头瘤病毒（HPV）疫苗接种的效果。这些评估很大程度上依赖群体免疫，进而取决于自然获得性免疫，而人们对这一机制知之甚少。我们考虑了不同的获得性免疫机制，评估了荷兰不同疫苗接种策略对HPV-16和HPV-18传播以及宫颈癌发病率的影响。
我们使用了STDSIM微观模拟模型，并考虑了感染后获得性免疫的两种机制：（I）具有可变持续时间的完全免疫；（II）对再次感染的易感性逐渐降低。13至16岁的女孩在一次覆盖率为50%的一次性补种活动中接种疫苗（HPV-16的效力为94.7%，HPV-18的效力为92.3%），随后对12岁女孩进行年度接种（覆盖率为60%）。替代疫苗接种方案包括提高覆盖率（包括男孩）以及降低疫苗效力。
在机制I下，HPV-16发病率降低了64%，在机制II下降低了75%；HPV-18发病率分别降低了58%和73%，这些降低导致宫颈癌病例减少了48 - 56%。提高覆盖率可使HPV发病率降低超过96%。对男孩进行疫苗接种可使女性中HPV-16发病率降低79 - 89%，HPV-18发病率降低83 - 98%。
不同获得性免疫机制之间HPV疫苗接种的效果评估略有差异，但这些差异不太可能影响政策决策。也可以考虑对男孩进行疫苗接种，以进一步降低癌症发病率。
