Pathogenesis of NiV infection is still poorly understood. As the endothelium forms the primary barrier of the circulatory system, endothelial dysfunction during infection could broadly affect immune cell function by regulating cytokines, chemokines and cell receptors and influencing vascular permeability. To gain new insights into virus-host interaction, we analyzed the transcriptome signature of NiV infection in primary human umbilical vein endothelial cells (HUVECs). Among the ten most strongly upregulated genes 8 h after NiV infection, we identified CXCL10 (interferon gamma-induced protein 10, IP-10), a chemokine that promotes leukocyte trafficking by acting on T lymphocytes, NK and dendritic cells via its receptor CXCR3 [8] . In addition to its protective role during the viral infection, CXCL10 may enhance the severity of virus infection and cause neuronal apoptosis and calcium dysregulation [9, 10] and enhance autoreactive lymphoproliferation and brain injury [11] . We have confirmed secretion of CXCL10 by NiV-infected HUVECs by ELISA and showed that increased production of CXCL10 follows NIV replication in experimentally infected hamsters. Finally, we demonstrated production of CXCL10 in brain endothelial cells of patients with fatal acute NiV encephalitis. Altogether, these results suggest that CXCL10 may be an important regulator of NiV-induced pathogenesis as well as a potential marker for NiV infection.