These results suggest that NiV-infection in endothelial cells induces CXCL10 production both in vitro and in vivo and highlight the use of molecular profiling of virus-infected cells as a powerful tool to define novel mechanisms of virus-host cell interaction. As equilibrium in cytokine production is essential in the generation of the adequate immune response, CXCL10 overexpression may be crucial for the development of NiV-associated encephalitis and could be a target for therapeutic approaches.