{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T23:07:42Z","timestamp":1788476862108,"version":"build-2803163510"},"reference-count":79,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2023,9,1]],"date-time":"2023-09-01T00:00:00Z","timestamp":1693526400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    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\n                    <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n                    (\n                    <jats:italic>Mtb<\/jats:italic>\n                    )-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\n                    <jats:italic>Mtb<\/jats:italic>\n                    . Importantly, we found that K18-hACE2 transgenic mice infected with SCV2 one month before, or months after aerosol\n                    <jats:italic>Mtb<\/jats:italic>\n                    exposure did not display exacerbated\n                    <jats:italic>Mtb<\/jats:italic>\n                    infection-associated pathology, weight loss, nor did they have increased pulmonary bacterial loads. However, pre-existing\n                    <jats:italic>Mtb<\/jats:italic>\n                    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.\n                    <jats:italic>Mtb<\/jats:italic>\n                    -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\n                    <jats:italic>Mtb<\/jats:italic>\n                    infection in mice, but rather the inflammatory response generated by\n                    <jats:italic>Mtb<\/jats:italic>\n                    infection in the lungs at the time of SCV2 exposure restricts viral replication.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2023.1240419","type":"journal-article","created":{"date-parts":[[2023,9,1]],"date-time":"2023-09-01T03:09:01Z","timestamp":1693537741000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":25,"title":["Co-infection of mice with SARS-CoV-2 and Mycobacterium tuberculosis limits early viral replication but does not affect mycobacterial loads"],"prefix":"10.3389","volume":"14","author":[{"given":"Paul J.","family":"Baker","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eduardo 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