Abstract

Men who have sex with men (MSM) harbor the highest prevalence of anal and oral Human Papillomavirus (HPV) infection, particularly if HIV-infected. We investigated anal and oral HPV infections in HIV-infected and HIV-uninfected MSM, to assess concurrent (HPV detected at both sites, irrespective of the genotypes), and concordant infections (same genotype[s] detected at both sites). Matched anal and oral samples from 161 MSM (85 HIV-infected, and 76 HIV-uninfected) were tested with the Linear Array. Determinants of concurrent and concordant infections were evaluated using logistic regression. Anal infections were 4 to 7 times more frequent than oral infections in both study groups (p < 0.0001). Concurrent infections were not significantly different in HIV-infected (25.9%) and HIV-uninfected MSM (17.1%), p = 0.18. A concordant infection was found in 15 MSM (9.3%). Concordance was for one genotype in 14 individuals and for four genotypes in the remaining subject. In the overall population, only age was independently associated with a concurrent infection (AOR = 3.10, 95% CI: 1.34–7.19 for >39 vs. ≤39 years). None of the parameters of sexual behavior showed independent association with concordant infections. Among MSM, concordant anal and oral HPV infections do not seem to be explained by sexual behavior, but might derive from sequential acquisition by autoinoculation.

Highlights

  • Persistent infections by mucosal high-risk Human Papillomaviruses (HPVs) are known to cause cancer at several anatomic sites [1]

  • We found that prevalence of i) any type of HPV, ii) high-risk types and iii) HPV16 was significantly higher at anal than oral level, both among HIV-infected and HIV-uninfected Men who have sex with men (MSM)

  • Anal HPV was found to exceed oral HPV prevalence by 4 to 7 times. This is consistent with findings by others who compared anal vs. oral infection in MSM [16,17,18,19,20]

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Summary

Introduction

Persistent infections by mucosal high-risk Human Papillomaviruses (HPVs) are known to cause cancer at several anatomic sites [1]. Anal and oral HPV infections have been extensively investigated in different sexually active populations [2,3] The epidemiology of these two infections, separately, has been largely investigated, evidencing the role of sexual exposure in the acquisition and transmission dynamics, in groups with high frequency of sexual contacts, partners, and practices, such as men who have sex with men (MSM) [2,4]. Several studies have explored co-occurrence, type-specific concordance, and sequential acquisition of multisite HPV infections (oral and genital, anal and genital) among women and men who have sex with women, suggesting that infections at these sites may not be independent [6,7,8,9,10,11,12] They may result from sexual behavior, they may be consequent to autoinoculation from one anatomical site to the other [7,10,13]

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