To supervise how distinct human cell types mount virus-stimulated transcriptional responses, we assayed epithelial cells (HeLa; HL) and B-lymphocytes (Namalwa; NM) by functional multi-omics (RNA-seq, ChIP-seq, and DNaseI-seq), both under homeostasis (naïve) and upon sequential infection with Sendai virus (SVI; NM, HL; 0, 3, and 6 h), an agonist of IRF, NF-κB, and ATF/Jun signaling pathways [4, 51, 52] (Figs 1 and 2; Supplementary Figs S1–S14, and Supplementary Tables S1 and 2). The gene discussed is JUN; the disease is infection.