Mice infected with Mycobacterium tuberculosis are resistant to acute disease caused by secondary infection with SARS-CoV-2

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dc.contributor.authorRosas Mejia, Oscaren
dc.contributor.authorGloag, Erin S.en
dc.contributor.authorLi, Jianyingen
dc.contributor.authorRuane-Foster, Marisaen
dc.contributor.authorClaeys, Tiffany A.en
dc.contributor.authorFarkas, Danielaen
dc.contributor.authorWang, Shu-Huaen
dc.contributor.authorFarkas, Laszloen
dc.contributor.authorXin, Gangen
dc.contributor.authorRobinson, Richard T.en
dc.contributor.editorSalgame, Padminien
dc.date.accessioned2022-12-14T20:31:24Zen
dc.date.available2022-12-14T20:31:24Zen
dc.date.issued2022-03en
dc.date.updated2022-12-14T19:08:50Zen
dc.description.abstractMycobacterium tuberculosis (Mtb) and SARS-CoV-2 (CoV2) are the leading causes of death due to infectious disease. Although Mtb and CoV2 both cause serious and sometimes fatal respiratory infections, the effect of Mtb infection and its associated immune response on secondary infection with CoV2 is unknown. To address this question we applied two mouse models of COVID19, using mice which were chronically infected with Mtb. In both model systems, Mtb-infected mice were resistant to the pathological consequences of secondary CoV2 infection, and CoV2 infection did not affect Mtb burdens. Single cell RNA sequencing of coinfected and monoinfected lungs demonstrated the resistance of Mtb-infected mice is associated with expansion of T and B cell subsets upon viral challenge. Collectively, these data demonstrate that Mtb infection conditions the lung environment in a manner that is not conducive to CoV2 survival.en
dc.description.versionPublished versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.1371/journal.ppat.1010093en
dc.identifier.eissn1553-7374en
dc.identifier.issn1553-7366en
dc.identifier.issue3en
dc.identifier.orcidGloag, Erin [0000-0001-8895-3444]en
dc.identifier.otherPMC8946739en
dc.identifier.otherPPATHOGENS-D-21-02248 (PII)en
dc.identifier.urihttp://hdl.handle.net/10919/112890en
dc.identifier.volume18en
dc.language.isoenen
dc.publisherPLoSen
dc.relation.urihttps://www.ncbi.nlm.nih.gov/pubmed/35325013en
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectRare diseasesen
dc.subjectLungen
dc.subjectInfectious diseasesen
dc.subjectBiodefenseen
dc.subjectPreventionen
dc.subjectPneumoniaen
dc.subjectVaccine relateden
dc.subjectHIV/AIDSen
dc.subjectTuberculosisen
dc.subjectEmerging Infectious Diseasesen
dc.subjectPneumonia & Influenzaen
dc.subject2.1 Biological and endogenous factorsen
dc.subject2 Aetiologyen
dc.subject2.2 Factors relating to the physical environmenten
dc.subjectInfectionen
dc.subject3 Good Health and Well Beingen
dc.subject.meshAcute Diseaseen
dc.subject.meshAnimalsen
dc.subject.meshCOVID-19en
dc.subject.meshCoinfectionen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred C57BLen
dc.subject.meshMycobacterium tuberculosisen
dc.subject.meshSARS-CoV-2en
dc.titleMice infected with <i>Mycobacterium tuberculosis</i> are resistant to acute disease caused by secondary infection with SARS-CoV-2en
dc.title.serialPLoS Pathogensen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.otherJournal Articleen
dc.type.otherResearch Support, N.I.H., Extramuralen
dc.type.otherResearch Support, Non-U.S. Gov'ten
dcterms.dateAccepted2022-02-23en
pubs.organisational-group/Virginia Techen
pubs.organisational-group/Virginia Tech/Veterinary Medicineen
pubs.organisational-group/Virginia Tech/Veterinary Medicine/Biomedical Sciences and Pathobiologyen
pubs.organisational-group/Virginia Tech/All T&R Facultyen
pubs.organisational-group/Virginia Tech/Veterinary Medicine/CVM T&R Facultyen

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