Mary Wilson
Well-known member
Published: March 24, 2022
https://doi.org/10.1371/journal.ppat.1010093
Oscar Rosas Mejia, Erin S. Gloag, Jianying Li, Marisa Ruane-Foster, Tiffany A. Claeys, Daniela Farkas, Shu-Hua Wang, Laszlo Farkas, Gang Xin, Richard T. Robinson
Abstract
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.
Author summary
Mycobacterium tuberculosis (Mtb) and SARS-CoV-2 (CoV2) are distinct organisms which both cause lung disease. We report the surprising observation that Mtb-infected mice are resistant to secondary infection with CoV2, with no impact on Mtb burden and resistance associating with lung T and B cell expansion.
https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1010093
https://doi.org/10.1371/journal.ppat.1010093
Oscar Rosas Mejia, Erin S. Gloag, Jianying Li, Marisa Ruane-Foster, Tiffany A. Claeys, Daniela Farkas, Shu-Hua Wang, Laszlo Farkas, Gang Xin, Richard T. Robinson
Abstract
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.
Author summary
Mycobacterium tuberculosis (Mtb) and SARS-CoV-2 (CoV2) are distinct organisms which both cause lung disease. We report the surprising observation that Mtb-infected mice are resistant to secondary infection with CoV2, with no impact on Mtb burden and resistance associating with lung T and B cell expansion.
https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1010093
