Some of the genes that had already been implicated in the pathogenesis of Ebola hemorrhagic fever such as IL-6 and TNF-a [6, 11] were induced after 1 h, but returned towards basal levels of expression after 6 h. Indeed, whereas LPS stimulation resulted in the activation of a large subset of TNF-a related signaling pathways at the 6 h time point there were no common pathways identified in the Ebola-infected pathway ORA. Similar results were obtained in another study, during which primary human macrophages, exposed to Ebola VLP VP40-GP for 24 h, were characterized by IL-1b, IL-6, IL-8, RANTES, and TNF-a expression that also peaked at 1 h or 6 h before receding to base levels [19] . These results contradict observations in vivo, which demonstrated upregulation of cytokines for extended periods of time [6, 7, 8, 9, 10, 11] . It is plausible that the early cytokine peak observed following high MOI infections in vitro is only achieved at a later time during in vivo infection. Another possible explanation for this difference is the duration of stimuli and thereby the duration of responses. For instance, in vivo, progeny virions are continuously produced by ZEBOV-infected cells and will therefore bind to and enter additional target cells, resulting in continuous stimuli that may maintain cytokine production and facilitate prolonged activation. Therefore, our in vitro approach most likely yielded results that are indicative of what continuously occurs in vivo. That increased cellular gene expression levels result in increased protein concentrations within 6 h was previously demonstrated in a study that used human macrophages exposed to VLP VP40-GP and ELISA measuring protein levels of IL-1b, IL-6, IL-8, TNF-a [19] .