Elske Marra1, Chunqing Lin2, Gary M Clifford2. 1. Department of Infectious Diseases, Public Health Service Amsterdam, the Netherlands. 2. International Agency for Research on Cancer, Lyon, France.
Abstract
Background: Anal human papillomavirus (HPV) infection, most notably HPV16, the central cause of anal cancer, is increased by anal sexual intercourse and worsened by human immunodeficiency virus (HIV)-positivity. Methods: A systematic review and meta-analysis of type-specific anal HPV prevalence in men, compared according to sexual preference, HIV status, and, when available, anal cytopathology. Results: Seventy-nine eligible studies included: 1805 HIV-negative men who have sex with women (MSW), 924 HIV-positive MSW, 8213 HIV-negative men who have sex with men (MSM), and 12758 HIV-positive MSM. Irrespective of anal cytopathology, HPV16 prevalence was significantly higher in MSM than MSW, both among HIV-negative (14% vs 3%; prevalence ratio (PR) 4.7; 95% confidence interval [CI] 2.5-8.9) and HIV-positive men (30% vs 11%; PR = 2.8; 95% CI, 1.9-4.1). Likewise, HPV16 was significantly higher in HIV-positive than HIV-negative men, both among MSW (PR = 3.5; 95% CI, 1.6-7.7) and MSM (PR = 2.1; 95% CI, 1.8-2.5). Anal HPV16 prevalence was similar between HIV-positive MSW and HIV-negative MSM. For MSM, anal HPV16 prevalence was significantly higher from studies with anal cytopathology, suggesting population sampling effects. Conclusion: Sexual preference and HIV infection are independent strong determinants of male anal HPV16 infection, confirming HIV-positive MSM as priorities for anal cancer prevention.
Background: Anal human papillomavirus (HPV) infection, most notably HPV16, the central cause of anal cancer, is increased by anal sexual intercourse and worsened by human immunodeficiency virus (HIV)-positivity. Methods: A systematic review and meta-analysis of type-specific anal HPV prevalence in men, compared according to sexual preference, HIV status, and, when available, anal cytopathology. Results: Seventy-nine eligible studies included: 1805 HIV-negative men who have sex with women (MSW), 924 HIV-positive MSW, 8213 HIV-negative men who have sex with men (MSM), and 12758 HIV-positive MSM. Irrespective of anal cytopathology, HPV16 prevalence was significantly higher in MSM than MSW, both among HIV-negative (14% vs 3%; prevalence ratio (PR) 4.7; 95% confidence interval [CI] 2.5-8.9) and HIV-positive men (30% vs 11%; PR = 2.8; 95% CI, 1.9-4.1). Likewise, HPV16 was significantly higher in HIV-positive than HIV-negative men, both among MSW (PR = 3.5; 95% CI, 1.6-7.7) and MSM (PR = 2.1; 95% CI, 1.8-2.5). Anal HPV16 prevalence was similar between HIV-positive MSW and HIV-negative MSM. For MSM, anal HPV16 prevalence was significantly higher from studies with anal cytopathology, suggesting population sampling effects. Conclusion: Sexual preference and HIV infection are independent strong determinants of male anal HPV16infection, confirming HIV-positive MSM as priorities for anal cancer prevention.
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