Influenza coinfection inhibits control of mycobacterial infection in a human challenge model
File(s)
Published version
Author(s)
Type
Journal Article
Abstract
Mycobacterium tuberculosis infection is a dynamic continuum. Clinical outcomes reflect complex host
pathogen interactions. Epidemiological and animal studies have suggested influenza coinfection as a risk factor for progression from contained infection to active disease, but human studies have been lacking. Using a whole blood luminescent mycobacterial growth inhibition assay within a human influenza challenge study, we show that influenza infection reduces immunological control of mycobacterial growth. Transcriptome-wide RNA sequencing, cytokine and cellular analyses of subjects’ blood before and after influenza infection reveal that innate immune pathways, including type 1 interferon signalling, are activated by influenza but their subsequent responsiveness to
mycobacteria is reduced, with multiple genes’ responses to BCG lux infection repressed by influenza coinfection. Our data suggest that influenza infection impairs immune mechanisms that contain mycobacterial growth and may be a risk factor for tuberculosis (TB) disease. Influenza vaccination might offer high risk, high prevalence populations protection against TB disease.
pathogen interactions. Epidemiological and animal studies have suggested influenza coinfection as a risk factor for progression from contained infection to active disease, but human studies have been lacking. Using a whole blood luminescent mycobacterial growth inhibition assay within a human influenza challenge study, we show that influenza infection reduces immunological control of mycobacterial growth. Transcriptome-wide RNA sequencing, cytokine and cellular analyses of subjects’ blood before and after influenza infection reveal that innate immune pathways, including type 1 interferon signalling, are activated by influenza but their subsequent responsiveness to
mycobacteria is reduced, with multiple genes’ responses to BCG lux infection repressed by influenza coinfection. Our data suggest that influenza infection impairs immune mechanisms that contain mycobacterial growth and may be a risk factor for tuberculosis (TB) disease. Influenza vaccination might offer high risk, high prevalence populations protection against TB disease.
Date Issued
2026-06-11
Date Acceptance
2026-03-31
Citation
Nature Communications, 2026, 17
ISSN
2041-1723
Publisher
Nature Portfolio
Journal / Book Title
Nature Communications
Volume
17
Issue
1
Copyright Statement
©The Author(s) 2026. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view acopyofthislicence, visit http://creativecommons.org/ licenses/by/4.0/.
License URL
Identifier
10.1038/s41467-026-72363-2
Publication Status
Published
Article Number
4884
Date Publish Online
2026-06-11