Pathway ORA of the data set for the 1 h Ebola-infected vs. mockinfected treatments identified a number of pathways directly related to activation of the G-protein coupled receptor pathway ( Table 1) . As chemokines and inflammatory mediators activate GPCR signaling this correlates with previous investigations demonstrating increased secretion of cytokines and chemokines following Ebola virus insult [16, 18] . It was also demonstrated that many of the genes identified as central nodes in the IPA functional networks (IL-6, IL-10, IRF-7, etc.) also occupied central positions in the signaling pathways identified with InnateDB (heterotrimeric GPCR signaling pathways). Indeed, the upregulation of pathways related to interleukin (IL)-2, IL-12, IL-23 and IL-27 signaling pathways were also identified as being differentially upregulated in Ebola-infected cells as compared to the mock-infected treatment (Table S1 ). Further, GPCR-related signaling pathways (cytokine-cytokine receptor interaction pathway) and the Jak-Stat signaling pathway were also upregulated during the immediate response to infection. Interestingly, pathways related to fibrinolysis (dissolution of fibrin clot pathway; fibrinolysis pathway) were also upregulated by Ebola infection as compared to the mockinfected control (Table 1) . Previously, dysregulation of the fibrinolytic system was recognized in Ebola-infected macaques [13] . A limited number of downregulated pathways were identified in our analysis as being significantly downregulated at 1 h post-infection and were largely related to metabolic processes as well as inhibition of the negative regulation of GPCR signaling (Table 1) .