期刊
SEXUALLY TRANSMITTED DISEASES
卷 40, 期 6, 页码 508-515出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/OLQ.0b013e318289c186
关键词
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资金
- National Cancer Institute, US National Institutes of Health [CA R01CA098803]
- Merck
- Sanofi-Pasteur MSD
- GSK
Background: Studies in women indicate that some sexually transmitted infections promote human papillomavirus (HPV) persistence and carcinogenesis. Little is known about this association in men; therefore, we assessed whether Chlamydia trachomatis (CT) infection and herpes simplex virus type 2 (HSV-2) serostatus are associated with genital HPV prevalence, an early event in HPV-related pathogenesis. Methods: Genital exfoliated cells, first-void urine, and blood from 3971 men recruited in the United States, Mexico, and Brazil were tested for HPV, CT, and HSV-2 antibodies, respectively. Multivariable logistic regression was used to assess the association of CT infection and HSV-2 serostatus with 4 HPV outcomes (any, oncogenic, nononcogenic only, and multiple infections). Results: A total of 64 (1.6%) men were CT positive, and 811 (20.4%) men were HSV-2 seropositive. After adjustment for potential confounders, CT was associated with any HPV (adjusted odds ratio [aOR], 2.19; 95% confidence interval [CI], 1.13-4.24), oncogenic HPV (aOR, 3.10; 95% CI, 1.53-6.28), and multiple HPV (aOR, 3.43; 95% CI, 1.69-6.95) prevalence. Herpes simplex virus type 2 serostatus was associated with any HPV (aOR, 1.25; 95% CI, 1.02-1.52), nononcogenic HPV only (aOR, 1.38; 95% CI, 1.08-1.75), and multiple HPV (aOR, 1.33; 95% CI, 1.06-1.68) prevalence. In analyses stratified by sexual behavior, CT infection was significantly associated with HPV detection among men reporting 2 or more recent sexual partners, whereas HSV-2 serostatus was significantly associated with HPV detection in men reporting 0 to 5 lifetime sexual partners. Conclusion: In this population, CT infection and HSV-2 serostatus were associated with prevalent genital HPV infection. Future prospective studies should investigate whether these infections influence HPV acquisition and/or persistence.
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