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Co-infection of mice with SARS-CoV-2 and limits early viral replication but does not affect mycobacterial loads. | LitMetric

Co-infection of mice with SARS-CoV-2 and limits early viral replication but does not affect mycobacterial loads.

Front Immunol

Inflammation and Innate Immunity Unit, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, United States.

Published: September 2023

AI Article Synopsis

Article Abstract

Viral co-infections have been implicated in worsening tuberculosis (TB) and during the COVID-19 pandemic, the global rate of TB-related deaths has increased for the first time in over a decade. We and others have previously shown that a resolved prior or concurrent influenza A virus infection in ()-infected mice resulted in increased pulmonary bacterial burden, partly through type I interferon (IFN-I)-dependent mechanisms. Here we investigated whether SARS-CoV-2 (SCV2) co-infection could also negatively affect bacterial control of . Importantly, we found that K18-hACE2 transgenic mice infected with SCV2 one month before, or months after aerosol exposure did not display exacerbated infection-associated pathology, weight loss, nor did they have increased pulmonary bacterial loads. However, pre-existing infection at the time of exposure to the ancestral SCV2 strain in infected K18-hACE2 transgenic mice or the beta variant (B.1.351) in WT C57Bl/6 mice significantly limited early SCV2 replication in the lung. -driven protection against SCV2 increased with higher bacterial doses and did not require IFN-I, TLR2 or TLR9 signaling. These data suggest that SCV2 co-infection does not exacerbate infection in mice, but rather the inflammatory response generated by infection in the lungs at the time of SCV2 exposure restricts viral replication.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10502726PMC
http://dx.doi.org/10.3389/fimmu.2023.1240419DOI Listing

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