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<p>Anal carcinoma is a relevant malignancy with increased incidence among people living with HIV (PLHIV), particularly in men who have sex with men (MSM) and transgender women (TW). Its main precursor lesion, high-grade anal intraepithelial neoplasia (HGAIN), is primarily associated with persistent infection with human papillomavirus (HPV). However, bacterial sexually transmitted infections (STIs) have been proposed as potential cofactors in anal carcinogenesis. The objectives of this study are to evaluate the relationship between asymptomatic bacterial anal STIs, the presence of HGAIN, and the diversity of oncogenic HPV genotypes in a cohort of MSM and TW living with HIV. A prospective study (June 2017–December 2023) was conducted at Son Llàtzer University Hospital (Palma de Mallorca, Spain), including 377 PLHIV (370 MSM, 7 TW). Anal cytology, detection of 14 oncogenic HPV genotypes, and screening for <i>Chlamydia trachomatis</i>,<i> Neisseria gonorrhoeae</i>,<i> and Mycoplasma genitalium</i> (from 2020 onward) were performed. Participants with abnormal cytology and/or HPV-16/18 underwent high-resolution anoscopy and biopsy. A total of 715 screening procedures were performed. Mean age was 44 years; 89% had an undetectable HIV viral load. The prevalence of bacterial STIs was 5.9% (<i>N</i> = 42/715) for <i>Chlamydia trachomatis</i>, 2.8% (<i>N</i> = 20/715) for <i>Neisseria gonorrhoeae</i>, and 10.3% (<i>N</i> = 45/438) for <i>Mycoplasma genitalium</i>. Oncogenic HPV was detected in 62.6% of samples, with HPV-16 being the most frequent genotype. Participants with bacterial STIs showed greater diversity of oncogenic HPV genotypes, particularly the association of <i>C. trachomatis</i> with HPV-16 and HPV-59, and <i>N. gonorrhoeae</i> with HPV-18, HPV-33 and HPV-68. Although no statistically significant differences in HGAIN rates were observed, individuals with bacterial STIs and high-risk HPV showed a numerically higher proportion of abnormal cytology. Asymptomatic bacterial anal STIs were common among MSM and TW living with HIV and were associated with greater oncogenic HPV diversity. Although no statistically significant association with HGAIN was demonstrated, the observed pattern may indicate that bacterial STIs influence HPV genotype distribution. Given the established role of specific high-risk genotypes, particularly HPV-16, in anal carcinogenesis, alterations in genotype distribution could theoretically contribute to carcinogenic pathways; however, no causal inference can be made, and longitudinal studies are needed to clarify their potential clinical implications. In this context, integrating bacterial STI screening into anal dysplasia surveillance programs may contribute to a more comprehensive approach to sexual health care in PLHIV.</p>

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Impact of bacterial sexually transmitted infections on human papillomavirus and anal dysplasia in people living with HIV

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月9日

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  • Aroa Villoslada,
  • Adrian Rodriguez,
  • Patricia Sorni,
  • Araceli Serrano,
  • Andrea Salom,
  • Carmen Collado,
  • Mercedes García-Gasalla,
  • Antoni Payeras

摘要

Anal carcinoma is a relevant malignancy with increased incidence among people living with HIV (PLHIV), particularly in men who have sex with men (MSM) and transgender women (TW). Its main precursor lesion, high-grade anal intraepithelial neoplasia (HGAIN), is primarily associated with persistent infection with human papillomavirus (HPV). However, bacterial sexually transmitted infections (STIs) have been proposed as potential cofactors in anal carcinogenesis. The objectives of this study are to evaluate the relationship between asymptomatic bacterial anal STIs, the presence of HGAIN, and the diversity of oncogenic HPV genotypes in a cohort of MSM and TW living with HIV. A prospective study (June 2017–December 2023) was conducted at Son Llàtzer University Hospital (Palma de Mallorca, Spain), including 377 PLHIV (370 MSM, 7 TW). Anal cytology, detection of 14 oncogenic HPV genotypes, and screening for Chlamydia trachomatis, Neisseria gonorrhoeae, and Mycoplasma genitalium (from 2020 onward) were performed. Participants with abnormal cytology and/or HPV-16/18 underwent high-resolution anoscopy and biopsy. A total of 715 screening procedures were performed. Mean age was 44 years; 89% had an undetectable HIV viral load. The prevalence of bacterial STIs was 5.9% (N = 42/715) for Chlamydia trachomatis, 2.8% (N = 20/715) for Neisseria gonorrhoeae, and 10.3% (N = 45/438) for Mycoplasma genitalium. Oncogenic HPV was detected in 62.6% of samples, with HPV-16 being the most frequent genotype. Participants with bacterial STIs showed greater diversity of oncogenic HPV genotypes, particularly the association of C. trachomatis with HPV-16 and HPV-59, and N. gonorrhoeae with HPV-18, HPV-33 and HPV-68. Although no statistically significant differences in HGAIN rates were observed, individuals with bacterial STIs and high-risk HPV showed a numerically higher proportion of abnormal cytology. Asymptomatic bacterial anal STIs were common among MSM and TW living with HIV and were associated with greater oncogenic HPV diversity. Although no statistically significant association with HGAIN was demonstrated, the observed pattern may indicate that bacterial STIs influence HPV genotype distribution. Given the established role of specific high-risk genotypes, particularly HPV-16, in anal carcinogenesis, alterations in genotype distribution could theoretically contribute to carcinogenic pathways; however, no causal inference can be made, and longitudinal studies are needed to clarify their potential clinical implications. In this context, integrating bacterial STI screening into anal dysplasia surveillance programs may contribute to a more comprehensive approach to sexual health care in PLHIV.