Fig. 5: HSV-1 infection activates cell signaling also in neighborhood.
From: Cellular state landscape and herpes simplex virus type 1 infection progression are connected
a ICP27, p-Akt (Ser473), p-ERK, and DAPI staining of HSV-1-infected HeLa cells at 12 hpi. Scale bar, 25 μm. b Density plots summarize single-cell mean intensities of p-Akt (Ser473) and p-ERK observed in different cell subpopulations from the smFISH + 4i experiment (0, mock cells; 1, uninfected cells without infected neighbors; 2, uninfected cells with infected neighbors; 3, infected cells). Data are from two (mock cells) or four (uninfected and infected cells) individual replicate wells. Cell counts are indicated in plots. c UMAP of mock- and HSV-1-infected HeLa cells at 12 hpi colored by cell subpopulations as in b (left), p-Akt (Ser473) (middle), or p-ERK (right). UMAP was computed using the same single-cell features as in Fig. 3a. Scale bar: lower limit is <0.5th and upper limit is >99.5th percentile of the values. Cell count is shown in the first UMAP. d Inhibition of ERK phosphorylation. HSV-1-infected HeLa cells were treated with DMSO or U0126 at 1.5 hpi, and ICP27 was detected using immunofluorescence imaging. Data are from two independent experiments and represent mean ± standard deviation among five replicate wells (2 or 3 replicate wells per experiment). Number of ICP27-expressing cells was compared between treatments within a time point or between time points within a treatment using two-sided unpaired two-sample t-test. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. 0.1–99.9th percentiles of marker intensities are shown in the density plots. See also Supplementary Figs. 8–11.
