Background: HIV-positive men who have sex with men (MSM) are at high risk of anal cancer compared with the general population. Human papillomavirus (HPV) infection, particularly HPV 16, is causally associated with anal cancer. However, the risk factors for anal HPV 16 infection are poorly understood. We determined the prevalence and risk factors for anal HPV 16 infection in a population of HIV-positive MSM, most of whom were being treated with antiretroviral therapy.
Design: Cross-sectional data from the baseline visit of a 4-year prospective cohort study.
Methods: Three hundred forty-eight HIV-positive MSM were recruited in San Francisco, and they received a detailed sexual behavior risk factor questionnaire. An anal swab was used to collect specimens for HPV type–specific DNA testing using L1 HPV DNA polymerase chain reaction. We used log-binomial multivariable models to determine the risk factors for anal HPV 16 infection.
Results: Ninety-two percent of HIV-positive MSM had at least 1 anal HPV type, 80% had at least 1 oncogenic HPV type, and 42% had HPV 16. Non-Hispanic white race and higher level of education were associated with a decreased risk of HPV 16 infection. A higher number of total male partners was associated with HPV 16 (relative risk: 1.6, 95% confidence interval 1.1 to 2.4, P = 0.01) for 201–1000 partners compared with 1–200. Injection drug use was independently associated with anal HPV 16 infection (relative risk: 1.5, 95% confidence interval 1.2 to 1.9, P = 0.003).
Conclusions: The prevalence of anal HPV infection, including HPV 16, is high in HIV-positive MSM. HIV-positive MSM should be counseled about the risk associated with increased partners and injection drug use.
*Department of Medicine, Division of Infectious Diseases, University of California, San Francisco, San Francisco, CA;
†Department of Epidemiology, School of Public Health, University of California, Berkeley, Berkeley, CA;
‡Center for Health Disparities Research and Department of Public Health, Brody School of Medicine, Greenville, NC;
§Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA; and
‖Department of Medicine, Division of Hematology and Oncology, University of California, San Francisco, San Francisco, CA.
Correspondence to: Alexandra L. Hernandez, PhD, MPH, Department of Medicine, Division of Infectious Diseases, University of California, San Francisco, Box 0654, 513 Parnassus Avenue, Room S420, San Francisco CA 94143 (e-mail: email@example.com).
Sources of support: (1) The study was conducted in the General Clinical Research Center, University of California, San Francisco, with funds provided by the Division of Research Resources 5 M01-RR-00079, US Public Health Service. The study was supported by NIH–NCI grant number R01CA54053. (2) A.L.H. was also supported through the University of California, Berkeley, Fogarty International AIDS/HIV International Training and Research grant (AITRP) 1-D43-TW000003.
The authors have no conflicts of interest to disclose.
All authors contributed to the interpretation of data and the overall intellectual content of the article, and drafting and editing of the manuscript. E.A.H. and J.M.P. contributed to the study design and data collection. A.L.H., J.T.E., and J.M.P. contributed to data analysis.
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Received November 21, 2012
Accepted March 29, 2013