Nasopharyngeal Microbiome Community Composition and Structure Is Associated with Severity of COVID-19 Disease and Breathing Treatment

Amy K Feehan,Julia Garcia-Diaz,Austin M Spitz,Rebecca Rose,Susanna L Lamers,Karlis Graubics,Rita R Colwell,David J Nolan

doi:10.3390/applmicrobiol1020014

Abstract

Viral infections are known to modulate the upper respiratory tract microbiome, but few studies have addressed differences in the nasopharyngeal microbiome following SARS-CoV-2 infection. Using nasopharyngeal swab medical waste samples from 79 confirmed SARS-CoV-2 positive and 20 SARS-CoV-2 negative patients, we assessed microbiome composition with metagenomic sequencing. COVID-19 status and breathing assistive device use was associated with differences in beta diversity, principal component analyses, community composition and abundance of several species. Serratia more frequently appeared in COVID-19 patient samples compared to negative patient samples, and Serratia, Streptococcus, Enterobacter, Veillonella, Prevotella, and Rothia appeared more frequently in samples of those who used breathing assistive devices. Smoking and age were associated with differences in alpha diversity. Cross-sectional differences in the microbiome were apparent with SARS-CoV-2 infection, but longitudinal studies are needed to understand the dynamics of viral and breathing treatment modulation of microbes.

Highlights

IntroductionIt is hypothesized that SARS-CoV-2 infection may compromise immunity and increase bacterial attachment, growth, and possibly lead to co-infections or “super infections” [5,6]
We examined the frequency with which particular genera were present or absent in patients for a subset of attributes: two that were hypothesized to be related to COVID-19 disease: (COVID-19 status, breathing assistance) and one that was hypothesized to be indirectly related
Genera that were observed in

Summary

Introduction

It is hypothesized that SARS-CoV-2 infection may compromise immunity and increase bacterial attachment, growth, and possibly lead to co-infections or “super infections” [5,6]. The microbiota is known to promote viral infections through several mechanisms including enhancement of virion stability [7,8], contributing to viral replication [9], and suppressing antiviral immunity [10]. Commensal microbiota can suppress viral infections directly by binding to viruses and thereby suppressing replication [11], destabilizing morphology [12], and/or inhibiting infectivity [13], or via other indirect mechanisms [14]. Interactions between the commensal microbiota and viral pathogens have been linked to clinical outcomes [8]

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Conclusion