ASSOCIATION OF ANAL DYSPLASIA AND HUMAN PAPILLOMAVIRUS WITH IMMUNOSUPPRESSION AND HIV-INFECTION AMONG HOMOSEXUAL MEN

Objective: To examine and quantify the association between anal squamous intraepithelial lesions (ASIL), anal human papillomavirus (HPV) infection and immunosuppression among HIV-seropositive and HIV-seronegative homosexual men. Design: Cross-sectional study among homosexual men presenting at a community-based clinic for HIV serologic screening. Results: Anal HPV DNA was detected in 55 and 23% of 285 HIV-seropositive and 204 HIV-seronegative men, respectively, by Southern transfer hybridization (STH) [odds ratio (OR), 4.0; 95% confidence interval (CI), 2.7-6.2], and in 92 and 78% by polymerase chain reaction (PCR) (OR, 3.1; 95% Cl, 1.6-5.8). ASIL was noted in 26% of HIV-seropositive men and in 8% of HIV-seronegative men (compared with men with negative cytologic findings: OR, 5.6; 95% Cl, 3.0-10.5), with high-grade lesions noted in 4% of HIV-seropositive and in 0.5% of HIV-seronegative men. Among HIV-infected men, ASIL, detection of specific anal HPV types, and detection of high levels of anal HPV DNA (i.e., levels of HPV DNA detectable by both STH and PCR) were all associated with immunosuppression. Nevertheless, HIV-seropositive men with CD4 counts > 500 x 10(6)/1 had a higher prevalence of both anal HPV and ASIL than men without HIV infection. Overall, detection of HPV at high levels was associated with ASIL. However, after adjustment for level of detectable HPV DNA, the risk of ASIL among HIV-seropositive men with CD4 counts < 500 x 10(6)/1 was increased 2.9-fold (95% Cl, 1.4-6.2) over that of HIV-seropositive men with CD4 counts > 500 x 10(6)/l. Conclusion: Given the high rates of ASIL in HIV-seronegative and both immunosuppressed and non-immunosuppressed HIV-seropositive homosexual men, natural history studies are now needed to assist in the development of strategies for the detection and management of such lesions. The increased prevalence of ASIL seen among immunosuppressed HIV-seropositive men may be the result of both a non-specific increase in productive HPV infection and HIV-induced immune alterations of HPV-related neoplasia.