The inflammatory cellular infiltrates found in the CNS of patients with acute NiV encephalitis include neutrophils, macrophages, lymphocytes and reactive microglia [7] , which may all play an important role in NiV pathogenesis. Recruitment of these cells indicates a possible action of chemokines, known as main regulators of leukocyte trafficking. Our analysis of the transcriptome profile of NiV-infected primary endothelial cells revealed the induction of several genes involved in the interferon type I pathway as well as the overexpression of CXCL10, an important chemoattractant chemokine with proinflammatory activity [19] .