The identified cellular genes whose expression levels were altered after exposure to Ebola virions belonged to different functional categories (Table S1 ). These genes include inflammatory cytokines, molecules that regulate blood coagulation (such as t-Pa, MMP-1, and serpine 1 and 2) genes involved in stressresponse, DNA repair, cell cycle arrest, and cell adhesion. In support of these functional categories, our pathway ORA also resulted in similar functional categorization of the differentially regulated signaling pathways following Ebola virus infection. The detection of a group of genes that responded to binding/entry of Ebola virions, VLP VP40-GP , as well as to LPS raises the question whether LPS and Ebola virions share receptors on the macrophage surface. Whereas receptors for Ebola virions on target cells remain elusive, it is known that LPS induces its effects by binding to TLR4 and MD2 and CD14 co-receptors. Recent studies demonstrated that Ebola VLP VP40-GP , but not VLP VP40 , induced cytokine and SOCS1 expression in a TLR4/MD2 dependent manner both in a human monocytic cell line (THP-1 cells) and in 293T cells expressing a functional TLR4/MD2 receptor [34] . The innate immune defense is achieved by activating NF-kB and type I IFN responses. It is already known that ZEBOV suppresses the host cell antiviral response by inhibiting interferon signaling via its VP35 and VP24 proteins [35, 36, 37, 38, 39, 40, 41] , and RNA silencing via VP35 [42] . Our studies revealed only limited IFN signaling in Ebola virion-exposed macrophages compared to those exposed to LPS, indicating that IFN signaling is inhibited early upon infection.