Fig. 1.

SARS-CoV-2 infection activates the cGAS-STING pathway. a, b Representative Western blots of STING and IRF3 phosphorylation upon SARS-CoV-2 infection (n = 2 independent experiments). Calu-3 (a) or HeLa-ACE2 (b) cells were mock-infected or infected with SARS-CoV-2 at an MOI of 0.5. At indicated time points after infection, cells were harvested and lysed. Lysates were then subjected to Western blot analysis using indicated antibodies. ✶Activated STING. c 2′3′-cGAMP levels in cells infected with SARS-CoV-2. HeLa-ACE2 were infected with SARS-CoV-2 as described in b. A competitive ELISA assay determined the 2′3′-cGAMP concentrations. Mean ± s.d., n = 3 independent experiments. **P < 0.01, n.s. not significant. Two-tailed Student’s t-test on log-transformed data. d STING and IRF3 phosphorylation upon SeV infection. HeLa-ACE2 cells were mock-infected or infected with SeV. Cells were harvested at indicated times and analyzed by Western blot. e Semi-quantitative analysis on Western blot results from a and d by densitometry. f Calu-3 cells were treated with DMSO or 200 ng/ml of H-151. After 2 h, cells were mock-infected or infected with SARS-CoV-2 at an MOI of 0.5 for 24 h. RNA extracted from the cells was evaluated by quantitative PCR. The data are expressed as fold change of the IFNB, IFIT1, ISG15, CCL5, and SARS-CoV-2 N mRNA levels relative to the GAPDH control. Mean ± s.d., n = 3 independent experiments. *P < 0.05, **P < 0.01, two-tailed Student’s t-test