In summary, an understanding of the mechanisms underlying Ebola virus-induced cytopathic effects has facilitated the process of vaccine and antiviral therapy development, which has in turn provided new information about pathogenesis and the immune response. Ebola virus does not exhibit the high degree of variability that other enveloped viruses may employ to evade host immunity, but Ebola virus GP alters target-cell function and exemplifies a novel strategy for immune evasion that may have arisen through the evolution of Ebola virus with its natural host. The cytotoxic effects of GP on macrophage and endothelial cell function disrupt inflammatory cell function and the integrity of the vasculature. In addition, by altering the cell surface expression of adhesion proteins and immune recognition molecules, Ebola virus may disrupt processes critical to immune activation and cytolytic-T-cell function. These phenomena likely account for the dysregulation of the inflammatory response and the vascular dysfunction characteristic of lethal Ebola virus infection, providing a rationale for focusing on GP as a target for a preventative vaccine and providing leads for other clinical interventions