Kenya Medical Research Institute, Center for Clinical Research, Kenya; Department of Global Health, University of Washington, Seattle, WA, USA; Partners in Health Research and Development, Kenya.
Department of Global Health, University of Washington, Seattle, WA, USA; Department of Obstetrics and Gynaecology, University of Washington, WA, USA.
Vaccine. 2021 Jul 30;39(33):4751-4758. doi: 10.1016/j.vaccine.2020.12.020. Epub 2021 Jan 21.
HIV infected children remain at increased risk of HPV associated malignancies as they initiate sexual activity. Though they mount a vigorous immune response to the quadrivalent human papillomavirus (QHPV-6, -11,-16, and -18; Gardasil®) vaccine, durability of the immune response is uncertain. We assessed antibody responses to HPV 6, -11, -16 and -18 for up to 48 months following administration of quadrivalent human papillomavirus vaccine in HIV-infected girls and boys ages 9-14 years in Kenya.
Of 178 girls and boys who had previously received three doses of the quadrivalent HPV vaccine, 176 enrolled into extended follow up for 4 years. HPV antibodies to -6, -11, -16 and -18 were measured at 24, 36 and 48 months after the first vaccine dose using the total immunoglobulin G immunoassay (IgG LIA). We evaluated the magnitude and trend in HPV vaccine response and the effect of plasma HIV-1 RNA on HPV vaccine response from month 24 to month 48 of follow up.
At re-enrollment, 24 months after initial vaccination, median age of participants was 14 years (range 11-17); 167 (95%) were receiving antiretroviral therapy and 110 (66%) had plasma HIV RNA < 40 copies/mL. The rate of HPV seropositivity at 48 months was 83% for HPV-6; 80% for HPV-11; 90% for HPV-16; and 77% for HPV-18. There was a plateau in mean log10 HPV-specific antibody titer between month 24 and 48. The mean log10 HPV-type specific antibody titer for children with undetectable HIV viral load (<40) at the time of vaccination consistently remained higher for the 48 months of follow up compared to children with detectable viral load.
Children with HIV infection may retain long term antibody response following HPV immunization. Further work to define whether HIV-infected children are protected from HPV acquisition with low levels of HPV antibodies is needed.
由于 HIV 感染儿童开始性行为时仍存在 HPV 相关恶性肿瘤的风险增加。尽管他们对四价人乳头瘤病毒(HPV-6、-11、-16 和-18;加德西®)疫苗产生了强烈的免疫反应,但免疫反应的持久性尚不确定。我们评估了在肯尼亚接受过三剂四价 HPV 疫苗的 9-14 岁 HIV 感染女孩和男孩在接种四价 HPV 疫苗后长达 48 个月时对 HPV 6、-11、-16 和-18 的抗体反应。
在 178 名之前已接受过三剂四价 HPV 疫苗的女孩和男孩中,有 176 名在接种第一剂疫苗后 4 年延长了随访。在接种第一剂疫苗后 24、36 和 48 个月,使用总免疫球蛋白 G 免疫测定法(IgG LIA)测量针对 HPV-6、-11、-16 和-18 的 HPV 抗体。我们评估了 HPV 疫苗反应的幅度和趋势,以及从随访第 24 个月到第 48 个月时血浆 HIV-1 RNA 对 HPV 疫苗反应的影响。
重新入组时,接种初始疫苗后 24 个月,参与者的中位年龄为 14 岁(范围 11-17);167 名(95%)正在接受抗逆转录病毒治疗,110 名(66%)血浆 HIV RNA<40 拷贝/ml。48 个月时 HPV 血清阳性率为 HPV-6 为 83%;HPV-11 为 80%;HPV-16 为 90%;HPV-18 为 77%。在接种后 24 至 48 个月之间,HPV 特异性抗体滴度的平均对数 10 呈平台状。接种时血浆 HIV 病毒载量(<40)不可检测的儿童的 HPV 型特异性抗体滴度的平均对数 10 在随访的 48 个月中始终保持较高水平,高于可检测到病毒载量的儿童。
感染 HIV 的儿童在 HPV 免疫接种后可能保持长期抗体反应。需要进一步研究以确定 HIV 感染儿童是否具有低水平 HPV 抗体而免受 HPV 感染。