Microbiome analysis in individuals with human papillomavirus oral infection

Abstract 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 o...

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Main Authors: David Israel Escobar Marcillo, Grete Francesca Privitera, Francesca Rollo, Alessandra Latini, Eugenia Giuliani, Maria Benevolo, Massimo Giuliani, Barbara Pichi, Raul Pellini, Maria Gabriella Donà
Format: Article
Language:English
Published: Nature Portfolio 2025-01-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-024-81607-4
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author David Israel Escobar Marcillo
Grete Francesca Privitera
Francesca Rollo
Alessandra Latini
Eugenia Giuliani
Maria Benevolo
Massimo Giuliani
Barbara Pichi
Raul Pellini
Maria Gabriella Donà
author_facet David Israel Escobar Marcillo
Grete Francesca Privitera
Francesca Rollo
Alessandra Latini
Eugenia Giuliani
Maria Benevolo
Massimo Giuliani
Barbara Pichi
Raul Pellini
Maria Gabriella Donà
author_sort David Israel Escobar Marcillo
collection DOAJ
description Abstract 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.
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spelling doaj-art-5c1aa4d805fe4245a172279308d1a9452025-01-26T12:28:44ZengNature PortfolioScientific Reports2045-23222025-01-0115111310.1038/s41598-024-81607-4Microbiome analysis in individuals with human papillomavirus oral infectionDavid Israel Escobar Marcillo0Grete Francesca Privitera1Francesca Rollo2Alessandra Latini3Eugenia Giuliani4Maria Benevolo5Massimo Giuliani6Barbara Pichi7Raul Pellini8Maria Gabriella Donà9Section of Mechanisms, Biomarkers and Models, Department of Environment and Health, Istituto Superiore di SanitàBioinformatics Unit, Department of Clinical and Experimental Medicine, University of CataniaPathology Department, IRCCS Regina Elena National Cancer InstituteSTI/HIV Unit, San Gallicano Dermatological Institute IRCCSSTI/HIV Unit, San Gallicano Dermatological Institute IRCCSPathology Department, IRCCS Regina Elena National Cancer InstituteSTI/HIV Unit, San Gallicano Dermatological Institute IRCCSOtolaryngology Head Neck Surgery Department, IRCCS Regina Elena National Cancer InstituteOtolaryngology Head Neck Surgery Department, IRCCS Regina Elena National Cancer InstituteSTI/HIV Unit, San Gallicano Dermatological Institute IRCCSAbstract 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.https://doi.org/10.1038/s41598-024-81607-4
spellingShingle David Israel Escobar Marcillo
Grete Francesca Privitera
Francesca Rollo
Alessandra Latini
Eugenia Giuliani
Maria Benevolo
Massimo Giuliani
Barbara Pichi
Raul Pellini
Maria Gabriella Donà
Microbiome analysis in individuals with human papillomavirus oral infection
Scientific Reports
title Microbiome analysis in individuals with human papillomavirus oral infection
title_full Microbiome analysis in individuals with human papillomavirus oral infection
title_fullStr Microbiome analysis in individuals with human papillomavirus oral infection
title_full_unstemmed Microbiome analysis in individuals with human papillomavirus oral infection
title_short Microbiome analysis in individuals with human papillomavirus oral infection
title_sort microbiome analysis in individuals with human papillomavirus oral infection
url https://doi.org/10.1038/s41598-024-81607-4
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