Abstract

BackgroundHIV-positive patients carry an increased risk of HPV infection and associated cancers. Therefore, prevalence and patterns of HPV infection at different anatomical sites, as well as theoretical protection of nonavalent vaccine should be investigated. Aim was to describe prevalence and predictors of oral HPV detection in HIV-positive men, with attention to nonavalent vaccine-targeted HPV types. Further, co-occurrence of HPV DNA at oral cavity and at anal site was assessed.MethodsThis cross-sectional, clinic-based study included 305 HIV-positive males (85.9% MSM; median age 44.7 years; IQR: 37.4–51.0), consecutively observed within an anal cancer screening program, after written informed consent. Indication for anal screening was given by the HIV physician during routine clinic visit. Paired oral rinse and anal samples were processed for the all HPV genotypes with QIASYMPHONY and a PCR with MY09/MY11 primers for the L1 region.ResultsAt the oral cavity, HPV DNA was detected in 64 patients (20.9%), and in 28.1% of these cases multiple HPV infections were found. Prevalence of oral HPV was significantly lower than that observed at the anal site (p < 0.001), where HPV DNA was found in 199 cases (85.2%). Oral HPV tended to be more frequent in patients with detectable anal HPV than in those without (p = 0.08). Out of 265 HPV DNA-positive men regardless anatomic site, 59 cases (19.3%) had detectable HPV at both sites, and 51 of these showed completely different HPV types. At least one nonavalent vaccine-targeted HPV type was found in 17/64 (26.6%) of patients with oral and 199/260 (76.5%) with anal infection. At multivariable analysis, factors associated with positive oral HPV were: CD4 cells <200/μL (versus CD4 cells >200/μL, p = 0.005) and >5 sexual partners in the previous 12 months (versus 0–1 partner, p = 0.008).ConclusionsIn this study on Italian HIV-positive men (predominantly MSM), oral HPV DNA was detected in approximately one fifth of tested subjects, but prevalence was significantly lower than that observed at anal site. Low CD4 cell count and increasing number of recent sexual partners significantly increased the odds of positive oral HPV. The absence of co-occurrence at the two anatomical sites may suggest different routes or timing of infection.

Highlights

  • HIV-positive patients carry an increased risk of Human Papilloma Virus (HPV) infection and associated cancers

  • HIVpositive persons experience a 3-fold higher standardized incidence of head and neck squamous cell carcinoma (HNSCC) than general population [3], and about 50% of oro-pharyngeal squamous cell carcinoma (OSCC) are HPV-related tumours, as found in a large retrospective study that investigated the prevalence of HPV infection in cancer tissues from more than 1600 patients diagnosed in the UK during the last decade [4]

  • LR: HPV infection sustained by only low risk HPV types; HR: HPV infection sustained by at least one high risk HPV type; Negative: negative for intraepithelial lesion or malignancy; Atypical squamous cells of undetermined significance (ASC-US): atypical squamous cells of undetermined significance; High grade squamous intraepithelial lesion (H-SIL): high grade squamous intraepithelial lesion atypia (ASC-US or more) was higher in presence of HR types when compared to subjects harbouring only LR types

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Summary

Introduction

HIV-positive patients carry an increased risk of HPV infection and associated cancers. Among non-AIDS cancers, HPV-associated tumours recently gained great attention because of multi-site distribution (genital tract, anus, head and neck), availability of screening procedures, and need of vaccine allocation strategies. HIVpositive persons experience a 3-fold higher standardized incidence of head and neck squamous cell carcinoma (HNSCC) than general population [3], and about 50% of oro-pharyngeal squamous cell carcinoma (OSCC) are HPV-related tumours, as found in a large retrospective study that investigated the prevalence of HPV infection in cancer tissues from more than 1600 patients diagnosed in the UK during the last decade [4]. Screening studies conducted in the HIV-infected population demonstrated an overall prevalence of HPV DNA in the oral cavity was between 20 and 45%, with the finding of the oncogenic type HPV16 between 12 and 26% [6,7,8,9]. Factors predictive of oral HPV infection were: HIV infection, severe immunodepression and number of sexual partners [9, 10]

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