a, Number of differentially expressed genes in structural cells after LCMV infection (this includes not only immune genes but also genes associated with the substantial organ-specific tissue damage and other direct and indirect effects of LCMV infection). b, Correlation of the observed changes in gene expression after LCMV infection across cell types and organs. c, Organ-specific viral load at day 8 of LCMV infection, measured by qPCR in whole-tissue samples collected from each organ (without FACS purification of individual cell types). Five reference genes were used for normalization and results were ranked across organs, to make the analysis robust towards tissue-specific differences in the expression of these housekeeping genes. However, the experimental results do not support an absolute quantification of viral load in each organ nor do they account for differences in the relative frequencies of cells that are susceptible to LCMV infection across organs. d, Scatterplot illustrating the low correlation between the activated epigenetic potential and the measured viral load across cell types and organs. e, f, Network analysis (e) and enrichment analysis (f) of potential cell–cell interactions between structural cells and haematopoietic immune cells, inferred from gene expression of known receptor–ligand pairs after LCMV infection (two-sided Fisher’s exact test with multiple-testing correction). For each combination of one structural cell type and one haematopoietic immune cell type, the analysis assesses whether all pairs of marker genes between the two cell types are enriched for annotated receptor–ligand pairs. Sample size (all panels): n = 3 independent biological replicates.