Effect of HIV infection on the natural history of anal human papillomavirus infection

被引:132
作者
Critchlow, CW
Hawes, SE
Kuypers, JM
Goldbaum, GM
Holmes, KK
Surawicz, CM
Kiviat, NB
机构
[1] Univ Washington, Sch Publ Hlth & Community Med, Dept Epidemiol, Human Papillomavirus Res Grp, Seattle, WA 98109 USA
[2] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98109 USA
[3] Univ Washington, Sch Med, Dept Med, Seattle, WA 98109 USA
[4] Univ Washington, Sch Med, Ctr AIDS & Sexually Transmitted Dis Res, Seattle, WA 98109 USA
[5] Seattle King Cty Dept Publ Hlth, Seattle, WA USA
关键词
HIV; human papillomavirus DNA; anal canal; longitudinal study; viral persistence; viral acquisition; homosexual men;
D O I
10.1097/00002030-199810000-00010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
Objective: To identify risk factors for the detection of prevalent and incident anal human papillomavirus (HPV) infection, and HPV persistence among HIV-seropositive and seronegative homosexual men. Design: Longitudinal study of 287 HIV-seronegative and 322 HIV-seropositive men attending a community-based clinic. Methods: Subjects underwent an interview and examination; specimens were collected for HIV serology and assessment of anal HPV and HIV DNA. Results: Anal HPV DNA was detected at study entry in 91.6% of HIV-infected men, and 65.9% of men not infected with HIV. HPV detection was associated with lifetime number of sexual partners and recent receptive anal intercourse (HIV-seronegative men), decreased CD4+ lymphocyte count (HIV-seropositive men), and anal warts (all men). Among men negative for HPV at study entry, subsequent detection of HPV was associated with HIV, unprotected receptive anal intercourse, and any sexual contact since the last visit. Among men positive for HPV at study entry, subsequent detection of additional HPV types was more common among HIV-seropositive men. Becoming HPV negative during follow-up was less common among men with HIV or high HPV levels at study entry. Among those with HIV, HPV persistence was associated with presence of anal HIV DNA, but not with CD4+ lymphocyte count. Conclusions: Risk of anal HPV infection appears to increase with sexual exposure, epithelial trauma, HIV infection and immune deficiency. Incident infection may result from recent sexual exposure or reactivation of latent infection. Further studies are needed to elucidate the mechanism by which HIV DNA in the anal canal increases the risk of HPV persistence. (C) 1998 Lippincott-Raven Publishers.
引用
收藏
页码:1177 / 1184
页数:8
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