DSouza Gypsyamber, Tewari Sakshi, Troy Tanya, Bleyer Paige, Korley Mabel, Kwait Jennafer, Ho Ken, Gillison Maura, Wiley Dorothy, Lazar Jason, Weber Kathleen M, Strickler Howard, Lahiri Cecile D, Palella Frank, Struijk Linda, Fakhry Carole
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, USA.
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, USA.
Oral Oncol. 2025 Apr;163:107249. doi: 10.1016/j.oraloncology.2025.107249. Epub 2025 Mar 17.
We evaluated incidence of oral HPV infection, which precedes HPV-related oropharynx cancer.
In this prospective multicenter cohort of participants with HIV and demographically similar participants without HIV, oral rinse and gargle samples were collected every 6-12 months and tested for 35 HPV types (anyHPV), 13 of which were oncogenic (oncHPV). Kaplan Meier and Cox regression were used for incidence curves and clustered risk factor hazard ratios. Logistic regression was used to determine relative odds of same infection at next visit.
The 1587 participants had a median follow-up of 3.67 years, 422 had 708 incident type-specific oral HPV detected. The most common oncHPV was HPV16 [incidence rate = 7.8 per 1000 person-years (95 %CI 5.8-10.6)]. At 5 years, the cumulative incidence of anyHPV, oncHPV and HPV16 was 34.9 % (95 %CI = 31.9 %, 38.3 %), 17.1% (95 %CI = 14.8 %, 19.8 %) and 4.0 % (95 %CI = 2.9, 5.6 %), respectively. Risk of incident oral HPV infection was independently associated with a higher number of oral sex partners, current smoking, younger age, prevalent oral anyHPV, living with HIV and lower CD4 counts. Prevalent oncHPV at baseline had greater odds of being re-detected at subsequent visits than an incident oncHPV detected for the first-time at a later visit. Detection of oral HPV type at one visit was associated with highly elevated odds of detecting that same type-specific infection at the next visit (OR > 100).
Cumulative incidence of oral HPV is increased among PLWH and with prevalent oral HPV, represents a mix of new and intermittently detected infections, and is higher among those with repeated detection of oral HPV.
我们评估了先于HPV相关口咽癌的口腔HPV感染发生率。
在这个针对HIV感染者以及人口统计学特征相似的非HIV感染者的前瞻性多中心队列研究中,每6 - 12个月收集一次口腔冲洗和漱口样本,并检测35种HPV类型(任何HPV),其中13种为致癌性(致癌HPV)。采用Kaplan - Meier法和Cox回归分析来绘制发病率曲线并计算聚集风险因素的风险比。使用逻辑回归来确定下次随访时相同感染的相对比值。
1587名参与者的中位随访时间为3.67年,422人有708次特定类型的口腔HPV感染事件被检测到。最常见的致癌HPV是HPV16[发病率 = 每1000人年7.8例(95%置信区间5.8 - 10.6)]。5年后,任何HPV、致癌HPV和HPV16的累积发病率分别为34.9%(95%置信区间 = 31.9%,38.3%)、17.1%(95%置信区间 = 14.8%,19.8%)和4.0%(95%置信区间 = 2.9,5.6%)。口腔HPV感染事件的风险与更多的口交性伴侣、当前吸烟、较年轻的年龄、口腔中存在任何HPV、感染HIV以及较低的CD4细胞计数独立相关。基线时存在的致癌HPV在后续随访中被重新检测到的几率高于在后期首次检测到的致癌HPV感染事件。在一次随访中检测到某种口腔HPV类型与在下一次随访中检测到相同类型特异性感染的几率大幅升高相关(比值比>一百)。
HIV感染者以及口腔中存在HPV的人群中口腔HPV的累积发病率增加,这代表了新感染和间歇性检测到的感染的混合情况,并且在多次检测到口腔HPV的人群中发病率更高。