Fig. 2

Broad and sustained interferon signatures in pathogenic SIV infection. A Boxplot depicting mean expression of all ISGs over time across all profiled cells. B Correlation between global IFN signature and viral load in each animal. C–D For each animal, within each cell type, and at each non-baseline time point, differentially expressed ISGs were calculated relative to pre-infection cells. C For each ISG, we calculated the mean number of time points at which that ISG was significantly upregulated (color of points). For each cell type, we calculated the number of ISGs significantly upregulated at any time point (size of points) and the cumulative log(fold-change) in expression of all significantly upregulated ISGs (y-axis). D For each ISG, animal class (170 or CL8), and cell type, we calculated the cumulative log(fold-change) of significantly upregulated ISGs across all cell types. Only ISGs with a cumulative log(fold-change) of > 0.75 in at least one animal group are shown. E In the two SIV-infected cell types (monocytes and CD4⁺ T cells), we calculated DEGs between SIV⁺ cells relative to SIV⁻ cells in CL8 animals (x-axis) and 170 animals (y-axis). F In monocytes (left) and CD4⁺ T cells (right), we calculated DEGs between SIV⁺ cells relative to SIV⁻ cells (y-axis). Then, among the SIV⁺ cells, we calculated DEGs between cells from 170-infected animals and cells from CL8-infected animals (x-axis). For C–F, all genes shown are significantly differentially expressed along at least one axis by Seurat’s implementation of the Wilcoxon rank-sum test