The Daffodil Centre, The University of Sydney, a Joint venture with Cancer Council NSW, Sydney, NSW, Australia; Melbourne School of Population and Global Health, University of Melbourne, Melbourne, Victoria, Australia.
Australian Centre for the Prevention of Cervical Cancer, 265 Faraday Street, Carlton South, Victoria, Australia; Department of Biochemistry and Pharmacology, University of Melbourne, Victoria, Australia; Department of Pathology, University of Malaya, Kuala Lumpur, Malaysia.
Tumour Virus Res. 2023 Jun;15:200255. doi: 10.1016/j.tvr.2023.200255. Epub 2023 Feb 1.
Australia's cervical screening program transitioned from cytology to HPV-testing with genotyping for HPV16/18 in Dec'2017. We investigated whether program data could be used to monitor HPV vaccination program impact (commenced in 2007) on HPV16/18 prevalence and compared estimates with pre-vaccination benchmark prevalence. Pre-vaccination samples (2005-2008) (n = 1933; WHINURS), from 25 to 64-year-old women had been previously analysed with Linear Array (LA). Post-vaccination samples (2013-2014) (n = 2989; Compass pilot), from 25 to 64-year-old women, were analysed by cobas 4800 (cobas), and by LA for historical comparability. Age standardised pre-vaccination HPV16/18 prevalence was 4.85% (95%CI:3.81-5.89) by LA; post-vaccination estimates were 1.67% (95%CI:1.21-2.13%) by LA, 1.49% (95%CI:1.05-1.93%) by cobas, and 1.63% (95%CI:1.17-2.08%) for cobas and LA testing of non-16/18 cobas positives (cobas/LA). Age-standardised pre-vaccination oncogenic HPV prevalence was 15.70% (95%CI:13.79-17.60%) by LA; post-vaccination estimates were 9.06% (95%CI:8.02-10.09%) by LA, 8.47% (95%CI:7.47-9.47%) by cobas and cobas/LA. Standardised rate ratios between post-vs. pre-vaccination rates were significantly different for HPV16/18, non-16/18 HPV and oncogenic HPV: 0.34 (95%CI:0.23-0.50), 0.68 (95%CI:0.55-0.84) and 0.58 (95%CI:0.48-0.69), respectively. Additional strategies (LA for all cobas positives; combined cobas and LA results on all samples) had similar results. If a single method is applied consistently, it will provide important data on relative changes in HPV prevalence following vaccination.
澳大利亚的宫颈癌筛查项目于 2017 年 12 月从细胞学转变为 HPV 检测,并对 HPV16/18 进行基因分型。我们研究了该项目的数据是否可用于监测 HPV 疫苗接种项目(2007 年启动)对 HPV16/18 流行率的影响,并将估计结果与疫苗接种前的基准流行率进行了比较。在疫苗接种前的样本(2005-2008 年)(n=1933;WHINURS)中,对 25-64 岁的女性进行了线性阵列(LA)分析。在疫苗接种后的样本(2013-2014 年)(n=2989;Compass 试点)中,对 25-64 岁的女性进行了 cobas 4800(cobas)分析,并对 LA 进行了历史可比性分析。LA 检测疫苗接种前 HPV16/18 的标准化流行率为 4.85%(95%CI:3.81-5.89);LA 检测疫苗接种后的估计值分别为 1.67%(95%CI:1.21-2.13%)、cobas 检测的 1.49%(95%CI:1.05-1.93%)、cobas 和 LA 检测非 16/18 cobas 阳性(cobas/LA)的 1.63%(95%CI:1.17-2.08%)。LA 检测疫苗接种前致癌 HPV 的标准化流行率为 15.70%(95%CI:13.79-17.60%);LA 检测疫苗接种后的估计值分别为 9.06%(95%CI:8.02-10.09%)、cobas 检测的 8.47%(95%CI:7.47-9.47%)和 cobas/LA。HPV16/18、非 16/18 HPV 和致癌 HPV 疫苗接种后与接种前的标准化率比值差异均有统计学意义:0.34(95%CI:0.23-0.50)、0.68(95%CI:0.55-0.84)和 0.58(95%CI:0.48-0.69)。采用其他方法(LA 用于所有 cobas 阳性;所有样本的 cobas 和 LA 联合检测结果)也得到了类似的结果。如果始终应用单一方法,则将提供有关 HPV 流行率在接种疫苗后发生相对变化的重要数据。