The endothelial cells represent one of the major targets of NiV infection, which is characterized by a systemic vasculitis and discrete parenchymal necrosis and inflammation in most organs, particularly in the central nervous system (CNS). The high pathogenicity of NiV infection appears to be primarily due to endothelial damage, syncytia and vasculitis-induced thrombosis, ischemia and vascular microinfarction in the CNS, allowing the virus to overcome the blood-brain-barrier (BBB) and to subsequently infect neurons and glia cells in the brain parenchyma [2, 7] .