哥斯达黎加HPV疫苗试验记录了二价HPV疫苗在疫苗接种后7年内对HPV31/33/45的交叉保护。即使是一剂疫苗。然而,这种保护的耐久性仍然未知。这里,我们评估了不同时间表的HPV31/33/45疫苗接种后11年的效力,扩展到其他非靶向HPV类型。
我们比较了接种疫苗妇女的HPV感染率与未接种疫苗妇女的类似队列中的感染率。我们估计了针对事件感染的平均疫苗效力(VEavg),并测试了VE随时间的变化。
在三剂女性中,我们观察到对HPV31/33/45的交叉保护具有统计学意义(VEavg=64.4%,95%置信区间[CI]=57.7%至70.0%)。此外,我们观察到了边界线,对HPV35的交叉保护具有统计学意义(VEavg=23.2%,95%CI=0.3%至40.8%)和HPV58(VEavg=21.2%,95%CI=4.2%至35.3%)。随着时间的推移,VE没有下降(HPV31、-33、-35、-45和-58的双侧P趋势>0.05)。作为一个基准,针对HPV16/18的VEavg为82.0%(95%CI=77.3%至85.7%)。在1剂女性中,我们观察到与HPV31/33/45的疗效相当(VEavg=54.4%,95%CI=21.0%至73.7%)。在接种疫苗和未接种疫苗的女性之间,获得未保护的HPV类型是相似的。表明HPV感染率的差异并非归因于生殖器HPV暴露的差异.
二价疫苗提供的针对HPV31/33/45的实质性交叉保护,并且在较小程度上,HPV35和HPV58在接种疫苗后11年持续并保持稳定,强化了二价疫苗是预防HPV相关癌症的有效选择的观点.
The Costa Rica HPV Vaccine
Trial has documented cross-protection of the bivalent HPV vaccine against HPV31/33/45 up to 7 years after vaccination, even with one dose of the vaccine. However, the durability of such protection remains unknown. Here, we evaluate the efficacy of different schedules of the vaccine against HPV31/33/45 out to 11 years postvaccination, expanding to other nontargeted HPV types.
We compared the rates of HPV infection in vaccinated women with the rates in a comparable cohort of unvaccinated women. We estimated the average vaccine efficacy (VEavg) against incident infections and tested for a change in VE over time.
Among 3-dose women, we observed statistically significant cross-protection against HPV31/33/45 (VEavg = 64.4%, 95% confidence interval [CI] = 57.7% to 70.0%). Additionally, we observed borderline, statistically significant cross-protection against HPV35 (VEavg = 23.2%, 95% CI = 0.3% to 40.8%) and HPV58 (VEavg = 21.2%, 95% CI = 4.2% to 35.3%). There was no decrease in VE over time (two-sided Ptrend > .05 for HPV31, -33, -35, -45, and -58). As a benchmark, VEavg against HPV16/18 was 82.0% (95% CI = 77.3% to 85.7%). Among 1-dose women, we observed comparable efficacy against HPV31/33/45 (VEavg = 54.4%, 95% CI = 21.0% to 73.7%). Acquisition of nonprotected HPV types was similar between vaccinated and unvaccinated women, indicating that the difference in HPV infection rates was not attributable to differential genital HPV exposure.
Substantial cross-protection afforded by the bivalent vaccine against HPV31/33/45, and to a lesser extent, HPV35 and HPV58, was sustained and remained stable after 11 years postvaccination, reinforcing the notion that the bivalent vaccine is an effective option for protection against HPV-associated cancers.