It is likely that the increased levels of sGP that are produced immediately after infection masked the 7U EBOV infection, and, when combined with the lack of cytotoxic effects associated with the over expression of GP1,2, resulted in the earlier time frame of disease for 7U EBOV challenge (i.e., increased ability of the host immune system to defend against 8U EBOV) [46,49]. This evidence concerns the gene GTPBP1 and infection.