Type-specific human papillomavirus infections among young heterosexual male and female STI clinic attendees.
ABSTRACT Baseline genotype-specific human papillomavirus (HPV) prevalence rates and associated risk factors per gender enable future assessment of the impact of vaccination on HPV dynamics.
Before the start of national HPV vaccination for girls, data were collected cross-sectionally in nationwide Dutch sexually transmitted infections (STI) clinics among heterosexual males (n = 430) and females (n = 1136) aged 16 to 24 years. Self-collected vaginal or penile swabs were analyzed by a sensitive polymerase chain reaction (SPF10) and genotyped with line probe assay. Logistic regression was applied to estimate determinants of HPV prevalent infections.
HPV prevalence was 54% among males and 72% among females. High-risk (HR) HPV was present in males and females, 40% and 58%, respectively. Independent risk factors for HR-HPV infection were female gender, number of lifetime sex partners and a history of chlamydia or gonorrhea. In addition, not having a casual partner and consistent condom use were protective factors in women, but not in men. For low-risk (LR) HPV, the odds were smaller. Multiple HR-HPV and sexual risk behavior showed a stronger association compared with a single HR-HPV infection.
Prevalence of HR-HPV is high in both genders. Infection with multiple HR-HPV types was more associated with high-risk sexual behavior than infection with LR-HPV types or a single HR-HPV type.
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ABSTRACT: In view of possible type replacement upon introduction of human papillomavirus (HPV) vaccination, we aimed to explore patterns of type-specific clustering across populations with various background infection risks. A total of 3,874 women from 3 cross-sectional studies in the Netherlands (in 2007-2009) provided vaginal self-samples, which were tested for 25 HPV genotypes by a sensitive molecular assay (SPF10 line probe assay, DDL Diagnostic Laboratory, Voorburg, the Netherlands). The number of concurrent HPV infections per woman was studied by Poisson regression. Associations between HPV types were investigated by generalized estimating equation analyses. The prevalence of any HPV type was 14% in a population-based study, 54% in a chlamydia screening intervention study, and 73% in a study among attendees of sexually transmitted infection clinics. Overall, multiple HPV infections were detected in 26% of the women. The number of concurrent HPV infections conformed to an overdispersed Poisson distribution, even after correction for known risk factors. Types differed significantly in their tendencies to be involved in coinfections, but no evidence for particular type-type interactions was found. Moreover, the strongest associations were observed in the lowest-risk population and vice versa.We found no indications of pairwise interactions, but our findings do suggest that clustering differs among HPV types and varies across risk groups.American journal of epidemiology 04/2014; DOI:10.1093/aje/kwu038 · 4.98 Impact Factor
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ABSTRACT: Objective Cervical cancer is caused by carcinogenic human papillomavirus (HPV) infections. Prior to the introduction of HPV vaccination in Suriname, we performed a cross-sectional study to estimate the prevalence of and determinants for genital carcinogenic HPV infections. Methods Women were recruited at a family planning (FP) clinic and a sexually transmitted infections (STI) clinic. Vaginal swabs were used for HPV genotyping by the SPF10 PCR-DEIA-LiPA(25) system. Logistic regression was used to identify determinants for carcinogenic HPV infection. Results The prevalence of any HPV was 54.2% and of carcinogenic HPV was 27.9% among 813 women attending the FP clinic. Among the 188 women attending the STI clinic, the prevalence of any HPV (76.1%) and of carcinogenic HPV (40.4%) was significantly higher. HPV52 was the most prevalent genotype in both clinics. The prevalence of HPV16 and/or 18 was 6.4% in the FP clinic and 12.2% in the STI clinic. The following determinants were independently associated with carcinogenic HPV infection among women visiting the FP clinic: >= 2 recent partners (OR 1.53; 95% CI 1.13 to 2.06), Chlamydia trachomatis co-infection (OR 1.89; 95% CI 1.32 to 2.70), disassortative ethnic sexual mixing (OR 1.50; 95% CI 1.13 to 1.99) and ethnic group (OR 1.90; 95% CI 1.27 to 2.85 for Creole and OR 1.67; 95% CI 1.06 to 2.62 for mixed ethnicity, both compared with Hindustani). No independent determinants were found among women visiting the STI clinic. Conclusions Carcinogenic HPV is highly prevalent among women in Suriname, and not equally distributed among ethnic groups. These data provide a baseline to assess possible shifts in the prevalence of HPV genotypes following vaccination.Sexually Transmitted Infections 06/2014; 90(8). DOI:10.1136/sextrans-2013-051384 · 3.08 Impact Factor
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ABSTRACT: To monitor the impact of human papillomavirus types 16 and 18 vaccine on HPV infection dynamics in the Netherlands, we started an ongoing study in sexually transmitted infection (STI) clinics in 2009. Here, we analyze baseline type-specific HPV DNA and HPV-specific antibody positivity rates. We enrolled 3569 men and women, 16-24 years of age, from 14 STI clinics, and estimated genital and anal HPV DNA and antibody positivity rates of 7 main carcinogenic HPV types. Generalized estimating equations regression analyses were applied to determine risk factors for, and associations between, type-specific HPV DNA and antibody positivity. Genital HPV DNA positivity rates were higher in women than in men; anal HPV DNA was especially high in men who have sex with men (MSM). HPV antibody seropositivity rates were also highest in women and MSM. High-risk sexual behavior was predictive of both HPV DNA and antibody positivity. Despite a strong correlation in serological profiles for multiple HPV types, seropositivity was independently associated with homologous HPV DNA detection. HPV DNA and antibody positivity rates are higher in women and MSM than in heterosexual men, but their association is similar across gender. This suggests a site-specific natural course of infection.PLoS ONE 04/2013; 8(4):e60696. DOI:10.1371/journal.pone.0060696 · 3.53 Impact Factor