Fig. 2: Fibrin drives lung pathology after SARS-CoV-2 infection.

a, Lung pathology of Beta-infected WT, Fga^−/− and Fgg^γ390–396A mice. b, Microscopy analysis of Mac2 (macrophages) and fibrin/fibrinogen in uninfected (UI) (n = 4) and Beta-infected WT (n =10), Fga^−/− (n = 10) and Fgg^γ390–396A (n = 9) mice; gp91^phox in uninfected (n = 3) and Beta-infected WT (n = 10), Fga^−/− (n = 10) and Fgg^γ390–396A (n = 9) mice; and Trichrome (collagen, blue; fibrin, red) in uninfected (n = 4) and Beta-infected WT (n = 5), Fga^−/− (n = 5), Fgg^γ390–396A (n = 4) mice. Data are from mice infected in two independent experiments. c, Gene set enrichment analysis (GSEA) of pathways significantly altered in Beta-infected lungs of Fga^−/− mice compared with WT mice. NES, normalized enrichment score. d, Significant genes and pathways. Uninfected: n = 4 (WT) and n = 3 (Fga^−/−) mice; Beta: n = 4 (WT) and n = 5 (Fga^–/–) mice. e, Microscopy analysis of NKp46, granzyme and spike in lung after infection. NKp46: uninfected, n = 8 (WT); infected, n = 10 (WT), n = 10 (Fga^−/−) and n = 9 (Fgg^γ390–396A) mice; granzyme: uninfected, n = 4 (WT); infected, n = 5 mice per group; spike: uninfected, n = 4 (WT); infected: n = 10 (WT), n = 10 (Fga^−/−) and n = 9 (Fgg^γ390–396A) mice. Statistical analysis was performed using one-way ANOVA with Tukey’s multiple-comparison test (b and e) and two-sided quasi-likelihood F-test implemented in edgeR (d). In d, bold font indicates adjusted P < 0.05 (Benjamini–Hochberg). Each lane represents the average scaled z-score for each genotype. Data are mean ± s.e.m. Scale bars, 100 μm (b and e). The diagram in a was created with BioRender.

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