Unveiling the role of the upper respiratory tract microbiome in susceptibility and severity to COVID-19
Otávio Von Ameln Lovison, Fabiana Caroline Zempulski Volpato, Lorenzo Gómez Weber, Afonso Luis Barth, Adriana Simon Coitinho, Andreza Francisco Martins
Frontiers in Cellular and Infection Microbiology, doi:10.3389/fcimb.2025.1531084
It is argued that commensal bacteria in the upper respiratory tract (URT) protect against pathogen colonization and infection, including respiratory viruses. Given that the microbiome can mediate immune modulation, a link between the URT microbiome (URTM) and COVID-19 susceptibility and severity is expected. This 16S metagenomics cross-sectional study assessed URTM composition, metabolic prediction, and association with laboratory biomarkers in non-COVID-19 pneumonia (NO-CoV), moderate (M-CoV), severe (S-CoV) COVID-19 patients, as well as COVID-19-negative, asymptomatic (NC) patients. The S-CoV group exhibited reduced URTM diversity, primarily due to a decreased abundance of eubiotic taxa. Some of these taxa (e.g., Haemophilus sp., Neisseria sp.) were also associated with inflammatory biomarkers. Multiple metabolic pathways (e.g., shortchain fatty acids, vitamin B12) linked to immune response, antiviral activity, and host susceptibility showed decreased abundance in S-CoV. These pathways could suggest potential alternatives for the therapeutic arsenal against COVID-19, providing reassurance about the progress in understanding and treating this disease.
Ethics statement The studies involving humans were approved by Comitêde E ́tica em Pesquisa do Hospital de Clıńicas de Porto Alegre. The studies were conducted in accordance with the local legislation and institutional requirements. The human samples used in this study were acquired from a by-product of routine care or industry. Written informed consent for participation was not required from the participants or the participants' legal guardians/next of kin in accordance with the national legislation and institutional requirements.
Author contributions
Conflict of interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Generative AI statement The author(s) declare that Generative AI was used in the creation of this manuscript. For english revision.
Publisher's note All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
Supplementary material The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fcimb.2025.1531084/ full#supplementary-material
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"abstract": "<jats:p>It is argued that commensal bacteria in the upper respiratory tract (URT) protect against pathogen colonization and infection, including respiratory viruses. Given that the microbiome can mediate immune modulation, a link between the URT microbiome (URTM) and COVID-19 susceptibility and severity is expected. This 16S metagenomics cross-sectional study assessed URTM composition, metabolic prediction, and association with laboratory biomarkers in non-COVID-19 pneumonia (NO-CoV), moderate (M-CoV), severe (S-CoV) COVID-19 patients, as well as COVID-19-negative, asymptomatic (NC) patients. The S-CoV group exhibited reduced URTM diversity, primarily due to a decreased abundance of eubiotic taxa. Some of these taxa (e.g., <jats:italic>Haemophilus</jats:italic> sp., <jats:italic>Neisseria</jats:italic> sp.) were also associated with inflammatory biomarkers. Multiple metabolic pathways (e.g., short-chain fatty acids, vitamin B12) linked to immune response, antiviral activity, and host susceptibility showed decreased abundance in S-CoV. These pathways could suggest potential alternatives for the therapeutic arsenal against COVID-19, providing reassurance about the progress in understanding and treating this disease.</jats:p>",
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