Open AccessMice infected with Mycobacterium tuberculosis are resistant to acute disease caused by secondary infection with SARS-CoV-2
Author(s) -
Oscar Rosas Mejia,
Erin S. Gloag,
Jianying Li,
Marisa Ruane-Foster,
Tiffany A. Claeys,
Daniela Farkas,
Shuhua Wang,
László Farkas,
Gang Xu,
Richard Robinson
Publication year - 2022
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1010093
Subject(s) - mycobacterium tuberculosis , tuberculosis , virology , immune system , biology , infectious disease (medical specialty) , disease , immunology , mycobacterium , microbiology and biotechnology , medicine , pathology
Mycobacterium 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.