Jair Kamwing, Abbott Stephen E, Aldous Annette, Rivas Karina I, Connors Kaleigh A, Klein David A, Hoke Elizabeth S, Jordan Jeanne A
George Washington University, School of Public Health, Department of Epidemiology, Washington, DC.
Whitman-Walker Health, Washington, DC.
J Low Genit Tract Dis. 2025 Jan 1;29(1):99-103. doi: 10.1097/LGT.0000000000000837. Epub 2024 Sep 11.
The aim of the study is to determine the prevalence of high-risk human papillomavirus (hrHPV) genotypes in men who have sex with other men and are living with HIV and the factors associated with anal high-grade squamous intraepithelial lesions (HSIL).
Anal swabs were collected for hrHPV genotyping from a cross-sectional group ( N = 163) of eligible men who have sex with other men and are living with HIV attending a high-resolution anoscopy clinic. Persistent hrHPV infections were studied in a longitudinal subset ( n = 37). Association of anal HSIL with specific hrHPV genotype(s) and with HIV-1 suppression was assessed. Pearson's χ 2 test with continuity correction or Fisher's exact test was used to determine statistical significance (alpha = 0.05).
Overall prevalence of hrHPV anal infections was 93.3% (152/163). Higher numbers of hrHPV genotypes were detected per sample in the HSIL group compared with less than or low-grade squamous intraepithelial lesion (≤LSIL) group ( p < .001). Proportion of participants infected with HPV33 was higher in the HSIL group (66.7%) than in ≤LSIL group (33.3%, p < .001), as was HPV35 (61.1% vs. 38.9%, p = .001) and HPV56 (56.7% vs. 43.3%, p = .022). HPV33 persistence was highly associated with HSIL (100%; 8/8) compared with ≤LSIL (0%; 0/8) ( p < .001). Proportion of HIV-1 suppression (<200 cp/mL) was significantly lower among the HSIL group (80%; 48/60) compared with ≤LSIL group (95.1%; 97/102) ( p = .006).
Statistically significant associations existed between anal HSIL and HPV33, HPV35, and HPV56 infections, with HPV33 persistence, and with the lack of HIV-1 suppression. These findings emphasize the critical need for genotyping assays that differentiate more than just HPV16, HPV18 and a pool of "other" hrHPV genotypes and that have an intended use with anal specimens. Globally, this highest-risk population would benefit from the 9-valent vaccine to prevent infections and reduce anal cancer risk.
本研究旨在确定男男性行为者且感染人类免疫缺陷病毒（HIV）人群中高危型人乳头瘤病毒（hrHPV）基因型的流行情况以及与肛管高级别鳞状上皮内病变（HSIL）相关的因素。
从一家高分辨率肛门镜检查诊所选取符合条件的男男性行为且感染HIV的横断面研究组（N = 163），采集肛门拭子进行hrHPV基因分型。在一个纵向亚组（n = 37）中研究持续性hrHPV感染情况。评估肛管HSIL与特定hrHPV基因型以及与HIV-1病毒抑制之间的关联。采用连续性校正的Pearson卡方检验或Fisher精确检验来确定统计学显著性（α = 0.05）。
hrHPV肛门感染的总体患病率为93.3%（152/163）。与低度或低级别鳞状上皮内病变（≤LSIL）组相比，HSIL组每个样本检测到的hrHPV基因型数量更多（p <.001）。HSIL组中感染HPV33的参与者比例（66.7%）高于≤LSIL组（33.3%，p <.001），HPV35也是如此（61.1%对38.9%，p =.001），HPV56同样（56.7%对43.3%，p =.022）。与≤LSIL组（0%；0/8）相比，HPV33持续性感染与HSIL高度相关（100%；8/8）（p <.001）。与≤LSIL组（95.1%；97/102）相比，HSIL组中HIV-1病毒抑制（<200拷贝/毫升）的比例显著更低（80%；48/60）（p =.006）。
肛管HSIL与HPV33、HPV35和HPV56感染、HPV33持续性感染以及缺乏HIV-1病毒抑制之间存在统计学显著关联。这些发现强调了对基因分型检测的迫切需求，这种检测不仅能区分HPV16、HPV18和一组“其他”hrHPV基因型，而且适用于肛门标本。在全球范围内，这一最高风险人群将从九价疫苗中受益，以预防感染并降低肛管癌风险。
