The pulmonary inflammatory microenvironment at the time of exposure governs innate control of SARS-CoV-2 replication
SARS-CoV-2 (SCV2) infection leads to diverse clinical outcomes ranging from asymptomatic to fatal disease. Co-morbidities, age and host genetics together with immune status affect disease severity.  However, the range of innate inflammatory pathways critical for limiting early viral replication and whether the inflammatory history and milieu of the lung microenvironment at the time of exposure impacts early control of SCV2 infection remain largely unexplored. Here, we investigated the roel of prior TLR stimualtion on early viral rpelciation in the lungs of K18 mice Overall design: Male JAX 34860 (K18-hACE2 Tg) mice, 10-15weeks old, infected with USA-WA1000TCIDd50