The commonality of these DEGs regardless of host or filovirus indicates a functional conservation of both mammalian defense mechanisms, such as IFN signaling, T cell activation and apoptosis, and viral infection mechanisms, such as IFN antagonism, even when certain mechanisms may differ molecularly (e.g., antagonism by EBOV VP24 but by MARV VP40 (67, 90, 91)). The gene discussed is IFNA1; the disease is viral infectious disease.