Matthew S Kelly, Pixu Shi, Sefelani C Boiditswe, Emily Qin, Andrew P Steenhoff, Tiny Mazhani, Mohamed Z Patel, Coleen K Cunningham, John F Rawls, Kathy Luinstra, Jodi Gilchrist, Julia Maciejewski, Jillian H Hurst, Patrick C Seed, David Bulir, Marek Smieja
{"title":"The role of the microbiota in respiratory virus-bacterial pathobiont relationships in the upper respiratory tract.","authors":"Matthew S Kelly, Pixu Shi, Sefelani C Boiditswe, Emily Qin, Andrew P Steenhoff, Tiny Mazhani, Mohamed Z Patel, Coleen K Cunningham, John F Rawls, Kathy Luinstra, Jodi Gilchrist, Julia Maciejewski, Jillian H Hurst, Patrick C Seed, David Bulir, Marek Smieja","doi":"10.1101/2024.10.22.24315478","DOIUrl":null,"url":null,"abstract":"<p><p>The mechanisms by which respiratory viruses predispose to secondary bacterial infections remain poorly characterized. Using 2,409 nasopharyngeal swabs from 300 infants in Botswana, we performed a detailed analysis of factors that influence the dynamics of bacterial pathobiont colonization during infancy. We quantify the extent to which viruses increase the acquisition of <i>Haemophilus influenzae</i> , <i>Moraxella catarrhalis</i> , and <i>Streptococcus pneumoniae</i> . We provide evidence of cooperative interactions between these pathobionts while identifying host characteristics and environmental exposures that influence the odds of pathobiont colonization during early life. Using 16S rRNA gene sequencing, we demonstrate that respiratory viruses result in losses of putatively beneficial <i>Corynebacterium</i> and <i>Streptococcus</i> species that are associated with a lower odds of pathobiont acquisition. These findings provide novel insights into viral-bacterial relationships in the URT of direct relevance to respiratory infections and suggest that the URT bacterial microbiota is a potentially modifiable mechanism by which viruses promote bacterial respiratory infections.</p>","PeriodicalId":94281,"journal":{"name":"medRxiv : the preprint server for health sciences","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11537323/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"medRxiv : the preprint server for health sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2024.10.22.24315478","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The mechanisms by which respiratory viruses predispose to secondary bacterial infections remain poorly characterized. Using 2,409 nasopharyngeal swabs from 300 infants in Botswana, we performed a detailed analysis of factors that influence the dynamics of bacterial pathobiont colonization during infancy. We quantify the extent to which viruses increase the acquisition of Haemophilus influenzae , Moraxella catarrhalis , and Streptococcus pneumoniae . We provide evidence of cooperative interactions between these pathobionts while identifying host characteristics and environmental exposures that influence the odds of pathobiont colonization during early life. Using 16S rRNA gene sequencing, we demonstrate that respiratory viruses result in losses of putatively beneficial Corynebacterium and Streptococcus species that are associated with a lower odds of pathobiont acquisition. These findings provide novel insights into viral-bacterial relationships in the URT of direct relevance to respiratory infections and suggest that the URT bacterial microbiota is a potentially modifiable mechanism by which viruses promote bacterial respiratory infections.