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Background Infection with human papillomaviruses (HPVs) can cause benign and malignant tumours in the anogenital tract and the oropharynx both in men and women. The aim of the presented study was to investigate cervical, anal, and oral HPV-detection rates among women referred to colposcopy for abnormal Cervical Cancer (CaCx) screening results and assess the concordance of HPV-types among these anatomical sites. Methods Women referred to colposcopy at a single centre due to abnormal cytology, conducted for CaCx screening, were subjected to cervical Liquid-based Cytology (LBC) smear testing, anal and oral sampling. Routine colposcopy consisted in multiple biopsies and/or Endocervical Curettage (ECC). HPV-detection was performed by PCR genotyping in all three anatomical sites. In high-risk (hr) HPV-DNA positive samples either from anal canal or oral cavity, anal LBC cytology and anoscopy were performed, or oral cavity examination respectively. Descriptive statistics was used for the analysis of HPV-detection rates and phi-coefficient for the determination of HPV-positivity concordance between the anatomical sites. Results Out of 118 referred women, hr. HPV-DNA was detected in 65 (55.1%), 64 (54.2%) and 3 (2.5%) at cervix, anal canal and oral cavity respectively while low-risk HPV-DNA was detected in 14 (11.9%) and 11 (9.3%) at cervix and anal canal respectively. The phi-coefficient for cervix/anal canal was 0.392 for HPV16, 0.658 for HPV31, 0.758 for HPV33, − 0.12 for HPV45, 0.415 for HPV52 and 0.473 for HPV58. All values were statistically significant ( p  < 0.001). Conclusions The results suggest that most HPV-types, high-risk and low-risk, detected in the cervix of women with prevalent cervical dysplasia, correlate with the ones detected in their anal canal. This particularly applies for the HPV-types included in the nonavalent HPV-vaccine (HPVs 6/11/16/18/31/33/45/52/58).

Abstract Background We aimed to assess the incidence and clearance of anal high-risk human papillomavirus (hrHPV) infections and determinants thereof among human immunodeficiency virus (HIV)-negative men who have sex with men (MSM) over a period of up to 5 years. Methods From 2010 to 2015, HIV-negative MSM were followed every 6 months. Anal self-swabs were collected at inclusion and every 6 months thereafter, and were HPV genotyped using the SPF10-PCR DEIA/LiPA25-system-v1. Incidence rates (IRs) and clearance rates (CRs) of incident anal hrHPV infections were assessed by hrHPV type (types 16, 18, 31, 33, 45, 52, and 58). Determinants of transitions between uninfected and infected states were assessed by hrHPV type using a time-homogenous multi-state Markov model. Results This study included 713 HIV-negative MSM, with a median age of 37 years (interquartile range [IQR] 31–43) and a median number of study visits of 6 (IQR 2–7). The IRs of anal infections had a median of 5.2 per 100 person-years (range: 2.2–7.9) across types, with HPV16 having the highest IR. The CRs of incident anal hrHPV infections had a median of 53.7 per 100 person-years (range: 33.4–65.3) across types, with HPV16 having the lowest CR. Having had over 100 lifetime sex partners was significantly associated with incident anal hrHPV infections in multivariable analyses. Conclusions The high incidence and low clearance rates of anal HPV16 infection, compared to other hrHPV types, is consistent with HPV16 being implicated in the large majority of anal cancer cases. Compared to other anal high-risk human papillomavirus (hrHPV) types, anal HPV16 had the highest incidence and lowest clearance rates of hrHPV infections over 5 years among human immunodeficiency virus–negative men who have sex with men.

Background. The purpose of this study was to assess the risk of sequential acquisition of anal human papillomavirus (HPV) infection following a type-specific genital HPV infection for the 9-valent vaccine HPV types and investigate factors associated with sequential infection among men who have sex with women (MSW). Methods. Genital and anal specimens were available for 1348 MSW participants, and HPV genotypes were detected using the Roche Linear Array assay. Sequential risk of anal HPV infection was assessed using hazard ratios (HRs) among men with prior genital infection, compared with men with no prior genital infection, in individual HPV type and grouped HPV analyses. Results. In individual analyses, men with prior HPV 16 genital infections had a significantly higher risk of subsequent anal HPV 16 infections (HR, 4.63; 95% confidence interval [CI], 1.41-15.23). In grouped analyses, a significantly higher risk of sequential typespecific anal HPV infections was observed for any of the 9 types (adjusted HR, 2.80; 95% CI, 1.32-5.99), high-risk types (adjusted HR, 2.65; 95% CI, 1.26, 5.55), and low-risk types (adjusted HR, 5.89; 95% CI, 1.29, 27.01). Conclusions. MSW with prior genital HPV infections had a higher risk of a subsequent type-specific anal infection. The higher risk was not explained by sexual intercourse with female partners. Autoinoculation is a possible mechanism for the observed association.

Background. Human immunodeficiency virus (HIV)—infected individuals are at greater risk for human papillomavirus (HPV)—associated anal than oropharyngeal cancers. The prevalence of anal vs oral HPV infections is higher in this population, but whether this is explained by higher incidence or persistence is unknown. Methods. Oral rinse and anal swab samples were collected semiannually from 404 HIV-infected adults in Baltimore, Maryland. Samples were tested for 37 HPV types using PGMY09/11 primers and reverse line-blot hybridization. Risk factors for HPV persistence were explored using adjusted Wei-Lin-Weissfeld models. Results. The prevalence (84% vs 28%), incidence (145 vs 31 per 1000 person-months), and 12-month persistence (54% vs 29%) were higher for anal vs oral HPV infections, respectively (each P < .001). Heterosexual men had lower incidence of anal HPV than men who have sex with men and women, but a higher incidence of oral HPV infection (test of interaction P < 0.001). In adjusted analyses, risk factors for HPV persistence included prevalent vs incident (adjusted hazard ratio [aHR] = 4.0; 95% confidence interval [CI], 3.5—4.8) and anal vs oral HPV infections (aHR = 1.5; 95% CI, 1.2—1.9). Conclusions. The higher incidence and persistence of anal vs oral HPV infections likely contributes to the higher burden of anal as compared to oral HPV-associated cancers in HIV-infected individuals.

Over the last decades, the incidence of anal cancer has increased worldwide. The discovery of the HPV virus as its primary cause and the natural progression of the disease, involving precancerous lesions, have resulted in significant interest in screening for anal cancer. The use of cytology testing, high-risk HPV DNA research, high-resolution anoscopy, and their combination has been adopted with variable success in detecting anal HPV precancerous lesions. Various studies have been carried out to evaluate the sensitivity and specificity of these techniques in different populations. High-risk populations for developing anal cancer have been identified through study of incidence and prevalence. Therefore, different scientific societies and experts worldwide have provided different recommendations for screening, but a universal approach has not yet been established. The inhomogeneity of different risk groups, the variable accessibility to specifical techniques, and the lack of data regarding the cost–benefit ratio of screening are the main problems to address in order to define a consensus guideline acceptable worldwide. The purpose of this paper is to provide a comprehensive review of the literature on HPV precancerous lesions and its screening, particularly after the release of recent recommendations.

Prevalence of human papillomavirus (HPV) infections was assessed among 1033 young men who have sex with men (MSM) aged 18–26 years. HPV (any type) was detected in 742 (71.8%) anal specimens and 101 (9.8%) oral specimens. Although HPV was detected in specimens from both anatomical sites in 83 (8.0%) participants, type-specific concordance for at least 1 HPV type was found in only 35 (3.4%) participants. HIV and smoking were associated with higher prevalence at both sites and frequency of concordant types. Coinfections of identical HPV types were rare, suggesting independent infection events and/or different modes of clearance.

Human papillomaviruses (HPVs) commonly infect the anogenital mucosa; most infections are transient, but a fraction of those caused by high-risk (HR) types persist and may lead to anogenital cancer. The epidemiology of HPV genotypes in anal infections in groups at different risk for anal cancer has not been well described in Italy. This retrospective study reports the results of HPV DNA testing and complete genotyping performed on anal swabs from 691 female and male patients attending proctology clinics in Rome during 2012–2021; one-third had repeated testing. Cumulative HPV positivity in 1212 anal swabs was approximately 60%, was not age related, and showed an increasing trend over the study period. HPV rates differed significantly by sex and HIV status: HIV-negative women had the lowest (43.6%) and HIV-positive men the highest (83.5%) HPV prevalence. HIV-positive men had more oncogenic HPV genotypes detected, more multiple infections, and the highest frequency of persistent infections. Two-thirds of all infections were vaccine-preventable. This study found that anal HPV infection rates are still elevated and even increasing in groups at low and high risk of developing anal cancer. Prevention programs need to be improved to reduce rates of anal infection in young women and men.

Background Human papillomavirus (HPV) infection is associated with anal cancers and is more prevalent in gay, bisexual, and men who have sex with men (gbMSM), partly due to their vulnerability to HIV infection. Baseline HPV genotype distributions and risk factors can inform the design of next‐generation HPV vaccines to prevent anal cancer. Methods A cross‐sectional study was conducted among gbMSM receiving care at a HIV/STI clinic in Nairobi, Kenya. Anal swabs were genotyped using a Luminex microsphere array. Multiple logistic regression methods were used to identify risk factors for four HPV outcomes (any HPV, any HR‐HPV, and 4‐ and 9‐valent vaccine‐preventable HPVs). Results Among 115 gbMSM, 51 (44.3%) were HIV‐infected. Overall HPV prevalence was 51.3%; 84.3% among gbMSM living with HIV and 24.6% among gbMSM without HIV (p < 0.001). One‐third (32.2%) had HR‐HPV and the most prevalent vaccine‐preventable HR‐HPV genotypes were 16, 35, 45, and 58. HPV‐18 was uncommon (n = 2). The 9‐valent Gardasil vaccine would have prevented 61.0% of HPV types observed in this population. In multivariate analyses, HIV status was the only significant risk factor for any HPV (adjusted odds ratio [aOR]:23.0, 95% confidence interval [95% CI]: 7.3–86.0, p < 0.001) and for HR‐HPV (aOR: 8.9, 95% CI: 2.8–36.0, p < 0.001). Similar findings were obtained for vaccine‐preventable HPVs. Being married to a woman significantly increased the odds of having HR‐HPV infections (aOR: 8.1, 95% CI: 1.6–52.0, p = 0.016). Conclusions GbMSM living with HIV in Kenya are at higher risk of anal HPV infections including genotypes that are preventable with available vaccines. Our findings support the need for a targeted HPV vaccination campaign in this population. This study found that HIV‐infected gbMSMs had a significantly higher prevalence of HPV than those without HIV. The most common vaccine‐preventable HR‐HPV genotypes were 16, 35, 45, and 58. The 9‐valent Gardasil vaccine could have prevented 61.0% of HPV types observed in this population.

Objectives This study aims to investigate the association between CD4 + T cell count and combined antiretroviral therapy (cART) with the prevalence of anal human papillomavirus (HPV) infection among HIV-positive male cohort in China. Methods A survey was conducted in men from a HIV cohort in Taizhou, China between 2016 and 2019. A face-to-face questionnaire interview was administered, and an anal-canal swab was collected for HPV genotyping. Results A total of 766 HIV-positive men were recruited. The HPV prevalence was lower among those with increased CD4 + T cell count than those with decreased or unchanged (46.5 vs. 56.6%, p = 0.033) from baseline. In multivariable models, having the current CD4 + T cell count of 350–499 cells/µL (aOR 0.28, 95% CI 0.13–0.64), and of ≥ 500 cells/µL (aOR 0.26, 95% CI 0.11–0.60) were associated with lower prevalence of any type HPV infection compared with those with < 200 cells/µL. Having taken NVP + 3TC + AZT was inversely associated with any high-risk (HR)-HPV (aOR 0.47, 95% CI 0.25–0.90) and any low-risk (LR)-HPV infection (aOR 0.40, 95% CI 0.18–0.88), compared with those taking EFV + 3TC + TDF. Conclusions Increased CD4 + T cell count at follow-up was significantly associated with lower prevalence of anal HPV infection. Inverse associations between NVP + 3TC + AZT and HR-HPV or LR-HPV infecton were observed.

The carcinogenicity of HPV infection in the anogenital and oropharyngeal regions is broadly accepted. The aim of the study was to define risk factors for anal and oral HPV infections in high-risk patients with biopsy-proven severe cervical lesions (CIN2+). Altogether immunocompetent 473 females with CIN2+ were categorized into the study group and another 245 women into the control group. The strongest risk factor for anal HPV infection was the presence of cervical HPV infection (p < 0.001). Furthermore, ten or more lifetime sexual partners (p = 0.013), a sexual non-coital contact with the anal area (p < 0.001), and actively practicing anal-penetrative intercourse (p < 0.001) were significantly associated with anal HPV. A history of genital warts in the woman (p = 0.010) and the presence of genital warts in the male partner (p = 0.029) were found statistically significant for the risk of oral HPV infection. Our data suggest that the presence of HPV infection, especially high-risk genotypes, in one anatomical site poses the greatest risk for HPV infection in another anatomical site. The cervix is the main reservoir of infection, but the risk factors for anal and oral HPV infections are dissimilar according to different anatomical distances and more complex routes of transmission.