PT  - JOURNAL ARTICLE
AU  - Oscar Rosas Mejia
AU  - Erin S. Gloag
AU  - Jianying Li
AU  - Marisa Ruane-Foster
AU  - Tiffany A. Claeys
AU  - Daniela Farkas
AU  - Laszlo Farkas
AU  - Gang Xin
AU  - Richard T. Robinson
TI  - Mice infected with <em>Mycobacterium tuberculosis</em> are resistant to secondary infection with SARS-CoV-2
AID  - 10.1101/2021.11.09.467862
DP  - 2021 Jan 01
TA  - bioRxiv
PG  - 2021.11.09.467862
4099  - http://biorxiv.org/content/early/2021/11/10/2021.11.09.467862.short
4100  - http://biorxiv.org/content/early/2021/11/10/2021.11.09.467862.full
AB  - 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 secondary CoV2 infection and its pathological consequences, 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.Competing Interest StatementThe authors have declared no competing interest.