RNA-seq of whole lungs from Irgm1-/- and wildtype littermates mice that were either uninfected or infected with influenza for 3, 6, or 10 days

We found that a dose of influenza (5,000 pfu of recombinant influenza A/WSN/33 (rWSN) H1N1 virus strain) that resulted in 50% mortality in wildtype littermate control mice showed minimal mortality in Irgm1-/- mice, indicating that Irgm1 deficiency was protective during influenza infection. This protective effect was dependent on the Type I interferon receptor Ifnar. We performed transcriptional profiling to identify molecular mechanisms associated with protection from influenza infection in Irgm1-/- lung. Both male and female mice were used at 8-12 weeks of age. Lung gene expression was assessed by RNA-seq at the following times post-influenza infection: Day 3 (early time point, early histological damage present in control mice), Day 6 (intermediate time point, late histological damage present in control mice) and Day 10 (late time point, morbidity and mortality present in control mice).