P10.13 Prevalence and predictors of high-risk anal human papillomavirus (hpv) types in the study of the prevention of anal cancer (spanc)

Introduction HPV causes ~90% of anal cancers, with HPV16 predominating. Gay men, particularly HIV-positive men, are at greatly increased risk of anal cancer. We describe prevalence and predictors of anal canal detection of any HPV, high-risk (hr) HPV and HPV16, in a cohort of Australian gay men. Methods SPANC is a 3-year community-recruited, prospective study of HIV(+) and HIV(-) gay men aged ≥35 years. At 6-monthly visits participants complete questionnaires, undergo high resolution anoscopy and anal swabs for cytology and HPV genotyping (Roche Linear Array). Results By December 2014, 482 participants (median age 49.5 years; 31% HIV positive) had attended a baseline visit. The majority (87%) had ≥1 HPV genotype detected, with ~ two thirds (65%) having ≥1 hrHPV detected. HPV16 was detected in 31% of participants. HIV positive participants and younger participants were more likely to have any HPV detected (p = 0.001 and p = 0.033 respectively). The detection of hrHPV in univariate analyses was significantly associated with positive HIV status (p = 0.001), currently smoking (p = 0.014), younger age (p = 0.012), more lifetime male sexual partners (p = 0.003), more lifetime receptive (RAI) and insertive (IAI) anal intercourse (p = 0.037 and p = 0.002 respectively) history of anal chlamydia (p = 0.003), more receptive anal behaviours in the last 6 months, including RAI (p HPV16 detection among HIV positive participants was four times more likely among men with a last CD4 cell count Conclusion Anal HPV was extremely common in this cohort of homosexual men. Prevalent HPV16 was related to low CD4 count in HIV positive men. Receptive anal sexual practices, including rimming and fingering were predictors of hrHPV detection. Disclosure of interest statement AEG has received honoraria and research funding from CSL Biotherapies, honoraria and travel funding from Merck, and sits on the Australian advisory board for the Gardasil HPV vaccine. CKF has received honoraria, travel funding and research funding from CSL and Merck, sits on the Australian advisory board for the Gardasil HPV vaccine, and owns shares in CSL Biotherapies. SMG has had grant support from CSL Bio and GlaxoSmithKline, and lecture fees from Merck, GlaxoSmithKline and Sanofi Pasteur; in addition, has received funding through her institution to conduct HPV vaccine studies for MSD and GlaxoSmithKline and is a member of the Merck Global Advisory Board as well as the Merck Scientific Advisory Committee for HPV. RJH has received support from CSL Biotherapies and MSD. All other authors declare that they have no conflicts of interest.