In contrast, differentially upregulated signaling responses at the 6 h time point were largely related to cell adhesion (syndecan-1-mediated signaling events), metabolism (prostaglandin and leukotriene metabolism; arachidonic acid metabolism; steroid hormone metabolism) and cytokine/chemokine signaling (cytokine-cytokine receptor interaction; chemokine signaling pathway; chemokine receptors bind chemokines) ( Table 2) . Interestingly, there was a large increase in the number of downregulated pathways at the 6 h time point as compared to the 1 h time point. Multiple pathways belonging to transcription and nucleotide/nucleoside metabolism were identified as being significantly downregulated in Ebola-infected cells as compared to the mock-infected controls 6 h post-infection ( Table 2) . Comparison of the differentially regulated pathway ORA data sets between the 6 h Ebola-infected vs. mock-infected and LPSstimulated vs. mock-stimulated treatments demonstrated minimal overlap of upregulated or downregulated pathways (data not shown). Whereas LPS stimulation resulted in the upregulation of pathways largely related to TNF-a, Toll-like receptor (TLR) or apoptosis signaling pathways these were not identified in the Ebola-infected samples. Thus, this likely indicates that the pro-inflammatory response to Ebola may be largely repressed by a yet unidentified mechanism at early time points following infection.