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<p>Microbiome gained attention as a cofactor in cancers originating from epithelial tissues. High-risk (hr)HPV infection causes oropharyngeal squamous cell carcinoma but only in a fraction of hrHPV+ individuals, suggesting that other factors play a role in cancer development. We investigated oral microbiome in cancer-free subjects harboring hrHPV oral infection (n = 33) and matched HPV− controls (n = 30). DNA purified from oral rinse-and-gargles of HIV-infected (HIV+) and HIV-uninfected (HIV−) individuals were used for 16S rRNA gene V3–V4 region amplification and sequencing. Analysis of differential microbial abundance and differential pathway abundance was performed, separately for HIV+ and HIV− individuals. Significant differences in alpha (Chao-1 and Shannon indices) and beta diversity (unweighted UniFrac distance) were observed between hrHPV+ and HPV-negative subjects, but only for the HIV− individuals. Infection by hrHPVs was associated with significant changes in the abundance of Saccharibacteria in HIV+ and Gracilibacteria in HIV− subjects. At the genus level, the greatest change in HIV+ individuals was observed for <i>Bulleidia</i>, which was significantly enriched in hrHPV+ subjects<i>.</i> In HIV− individuals, those hrHPV+ showed a significant enrichment of <i>Parvimonas</i> and depletion of <i>Alloscardovia</i>. Our data suggest a possible interplay between hrHPV infection and oral microbiome, which may vary with the HIV status.</p>

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Microbiome analysis in individuals with human papillomavirus oral infection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年1月23日

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  • David Israel Escobar Marcillo,
  • Grete Francesca Privitera,
  • Francesca Rollo,
  • Alessandra Latini,
  • Eugenia Giuliani,
  • Maria Benevolo,
  • Massimo Giuliani,
  • Barbara Pichi,
  • Raul Pellini,
  • Maria Gabriella Donà

摘要

Microbiome gained attention as a cofactor in cancers originating from epithelial tissues. High-risk (hr)HPV infection causes oropharyngeal squamous cell carcinoma but only in a fraction of hrHPV+ individuals, suggesting that other factors play a role in cancer development. We investigated oral microbiome in cancer-free subjects harboring hrHPV oral infection (n = 33) and matched HPV− controls (n = 30). DNA purified from oral rinse-and-gargles of HIV-infected (HIV+) and HIV-uninfected (HIV−) individuals were used for 16S rRNA gene V3–V4 region amplification and sequencing. Analysis of differential microbial abundance and differential pathway abundance was performed, separately for HIV+ and HIV− individuals. Significant differences in alpha (Chao-1 and Shannon indices) and beta diversity (unweighted UniFrac distance) were observed between hrHPV+ and HPV-negative subjects, but only for the HIV− individuals. Infection by hrHPVs was associated with significant changes in the abundance of Saccharibacteria in HIV+ and Gracilibacteria in HIV− subjects. At the genus level, the greatest change in HIV+ individuals was observed for Bulleidia, which was significantly enriched in hrHPV+ subjects. In HIV− individuals, those hrHPV+ showed a significant enrichment of Parvimonas and depletion of Alloscardovia. Our data suggest a possible interplay between hrHPV infection and oral microbiome, which may vary with the HIV status.