Fig. 2: Influenza A virus infection promotes dormant DCC proliferation and phenotypic change.

a,b, Immunofluorescence (a) and quantification (b) of Ki67⁺ HER2⁺ cells in lungs after IAV infection. Lung sections from naive and IAV-infected mice were stained with antibodies against HER2 (green), Ki67 (magenta) and DAPI (blue) (a). Percentage of Ki67⁺ HER2⁺ cells (b, left), absolute number of Ki67⁺ HER2⁺ cells across three lung sections (middle, n = 4 per group, n = 3 at 15 dpi) and detection of EdU incorporation (right, n = 3 per group). c,d, Immunofluorescence and quantification of vimentin⁺ (Vim⁺) (c) and EpCAM⁺ HER2⁺ (d) cells in lungs after influenza infections, in which lung sections from naive and IAV-infected mice were stained with HER2 (green) and vimentin (magenta) (n = 3 per group, n = 4 PBS, 9 dpi, 60 dpi) or HER2 (green) and EpCAM (magenta) (n = 3 per group). Graphs show the percentage of vimentin⁺ HER2⁺ (c) or EpCAM⁺ HER2⁺ (d) cells. In a–d, statistical significance relative to PBS samples is shown, as determined by one-way ANOVA. e, GSEA analyses comparing DCCs from lungs of uninfected (PBS) and IAV-infected MMTV-Her2 mice at 9 dpi. See Supplementary Fig. 2 for the gating strategy used for sorting. f–h, Heatmaps of significantly differentially expressed collagen (Col) isoforms/lysyl oxidase (f), metalloproteinase (Mmp) (g) and vascular endothelial growth factor (Vegf) and intercellular adhesion molecule (Icam)/vascular cell adhesion molecule-1 (Vcam1) genes (h). All box-and-whisker plots are presented as maximum value (top line), median value (middle line) and minimum value (bottom line) with all data points shown by dots. Scale bars: a, 25 μm; c and d, 10 μm. All replicates are biological.

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