Fig. 9

Effect of cGAS or STING deficiency on influenza virus replication in vivo. a, b WT mice were intranasally infected with 1,000 pfu of PR8 virus. The BAL fluids (a) and lung tissues (b) were collected at indicated time points. DNA was extracted from BAL fluids of mock- or influenza virus-infected mice using QIAquick Nucleotide Removal kit (QIAGEN). Cytosolic mtDNA was assessed by quantitative PCR (a). Total RNAs were extracted from the lung tissue of mock- or influenza virus-infected mice. IFN-β mRNA levels were assessed by quantitative PCR with GAPDH as an internal control (b). c, d WT, cGAS^−/−, Sting^gt/gt, and MAVS^−/− mice were intranasally infected with 1000 pfu of PR8 virus. Lung tissues were collected at 4 d post infection. Total RNAs were extracted from the lung tissue and IFN-β mRNA levels were assessed by quantitative PCR with GAPDH as an internal control. e WT (n = 37), cGAS^−/− (n = 18), Sting^gt/gt (n = 16), and MAVS^−/− (n = 10) mice were intranasally infected with 1000 pfu of PR8 virus. The BAL fluids were collected at 5 d post infection and viral titers were determined by standard plaque assay. These data are from three independent experiments (a–d; mean ± s.e.m.) or pooled from four independent experiments (e; mean ± s.e.m.). *P < 0.05, ***P < 0.001; (one-way ANOVA and Tukey’s test). Source data are provided as a Source Data file