The p38/MAPK pathway mediates the cellular response to environmental stress, pathogenic infection, and pro-inflammatory cytokine stimulation, whereas downstream effectors of the pathway include transcription factors and RNA binding proteins that promote inflammatory cytokine production (Cuadrado and Nebreda 2010; Wen et al., 2010). Analysis of estimated transcription factor activity from gene expression data (STAR Methods; Table S6) derived from the infection of a human lung carcinoma cell line (A549), a human epithelial lung cancer cell line (Calu3), and primary human bronchial epithelial (NHBE) cells demonstrated that transcription factors regulated by the p38/MAPK pathway were among the most highly activated upon infection (Figure 6E; Blanco-Melo et al., 2020).