Persistence and clearance of HPV infection at anal site in a cohort of HIV‐positive males

We aimed to assess the persistence and clearance of HPV‐DNA at anal site in a cohort of HIV‐positive patients (pts) asymptomatic for sexually transmitted diseases (STD). Consecutive HIV‐pos males underwent anoscopy, and each anal sample was analyzed for HPV‐PCR detection/genotyping (high‐risk genotypes: HR‐HPV) and for cytologic abnormalities (Bethesda System 2001: low and high grade SIL, LSIL‐HSIL). Immune activation in peripheral blood (CD8/CD38+) was assessed by flow cytometry. Pts were re‐examined at a 12–18 months follow‐up visit. Comparisons were assessed by Mann‐Whitney and chi‐square test. Factors related to HPV persistence were identified by logistic regression. 105 HIV‐pos males were studied: 89 (84%) were MSM, 76 (72%) were on HAART, median age was 42 (IQR:34–47), median CD4 count of 500 cell/mmc (IQR:366–680). HPV‐DNA was detected in anal swabs from 96 (91.4%) pts, 77 of them (80%) harbored HR‐HPV; 46 were coinfected with>1 HR‐HPV. Most frequent genotypes were HPV‐16 (30%), HPV‐58 (25%). In a median follow up of 18 months (IQR 12–24), 83/96 (86.4%) pts showed persistent HPV infection, while 13 (13.5%) became negative; conversely, 6 (5%) pts, HPV‐negative at baseline, acquired HPV infection. Younger pts and those with a shorter duration of HIV infection showed a higher prevalence of HPV persistence (Table). Conversely being on HAART and a longer duration of therapy were associated to viral clearance. Interestingly, pts with persistent HPV infection showed an activated immune profile at baseline, with significantly higher CD8+CD38+%. In the multivariate analysis only SIL at baseline (AOR 4.11, 95% CI 0.89–18.9, p=.06), being MSM (AOR 5.11, 95% CI 0.87–29.8, p=.06) and higher CD8+CD38+% (AOR 1.93, 95% CI 0.88–4.24, p=.09) were borderline associated with persistent anal HPV infection. Our results confirm a higher prevalence and persistence of anal HPV infection in HIV‐positive males; HIV‐pos pts with anal HPV infection should be thus strictly followed‐up for the early detection of pre‐cancerous lesions. Table Demographic characteristics of study population at baseline according to persistence of HPV infection Characteristics at baseline HPV+ pts that become negative at follow‐up (n=13) HPV+ pts that remain positive at follow‐up (n=83) p Age* 48 (42–60) 41 (33–46) 0.008 MSM° 9 (69%) 74 (89%) 0.071 HAART° 13 (100%) 57 (68%) 0.017 HAART duration (mths)* 121 (41.5–180) 46 (21.25–119.3) 0.030 HIV duration (mths)* 125 (56–202) 43 (22–130) 0.007 CD4+T cells/mmc* 525 (407–656) 500 (362–680) 0.59 Nadir CD4+T cells/mmc* 285 (173–403.5) 300 (163–396) 0.99 CD8+T cells/mmc* 846 (638–1008) 884 (748–1060) 0.26 HIV‐RNA cp/mL* 59 (39–59) 59 (39–16967) 0.15 CD8+CD37+% 1 (1–1) 2 (1–4) 0.003 Dysplasia 3 (23%) 52 (62.6%) 0.011 HR‐HPV° 8 (61.5%) 69 (83%) 0.12 Follow‐up duration (mths)* 18 (12.5–30) 18 (12–24) 0.58 Data are presented as the median (IQ R); °Data are presented as the number (percentage).