The host response to virulent pathogens is likely to fall into two categories [21] . First, there are common responses to unrelated pathogens, such as the type 1 IFN innate immune response that renders uninfected neighboring cells resistant to virus infection. Second, there are responses specific for individual pathogens. On the other hand, pathogens have evolved to counter these responses to ensure their own survival and transmission. Examples are how viruses of disparate families overcome the antiviral action of apolipoprotein B mRNA editing enzyme, catalytic polypeptidelike 3G (APOBEC3G) [43] , tripartite motif containing 5 (TRIM5a) [44] , bone marrow stromal cell antigen 2 (BST-2)/ tetherin [45, 46, 47] , or interferon induced transmembrane proteins (IFITM) [46, 48, 49] . It is important to remember that this study partially characterizes the response of humans to ZEBOV infection and that humans are not natural hosts of this virus. Therefore, host responses and virus counteractions are not in a state of equilibrium. It is therefore a fundamentally interesting question whether infected humans succumb to Ebola hemorrhagic fever because of direct effects exerted by the virus on the body or because of overbearing immune responses by the individual. Recently, various frugivorous bats have been implicated as potential filovirus reservoirs that seemingly remain unaffected by infection [50, 51] . It is therefore tempting to repeat our studies with cells from these animals to see whether their responses to Ebola virion exposure are fundamentally different.