Individual chemokines, including CXCL10, play opposing roles in neuroinflammation in different experimental models of infectious disease, making it difficult to predict whether they have a protective role by contributing to immune eradication of the microbial attack or they cause inflammatory damage and disease [19] . Therefore, potential effect of CXCL10 in NiV infection could be either beneficial or harmful and the balance between these two effects may be critical for the final outcome of the disease. Infection with RNA viruses that may cause encephalitis in humans, such as HIV or lymphocytic choriomeningitis viruses, or in rodent models, such as mouse hepatitis virus and Theiler's virus, can directly induce the expression of chemokines by astrocytes and microglia and establish chemokine gradients that promote leukocyte trafficking within the CNS [11, 31, 32, 33] . In addition, neutralization of CXCL10 decreased leukocyte migration to areas of infection in measles virus-infected brain tissue [34] . Although several of these viruses directly infect neurons, these cells have not been observed to participate in the inflammatory response, suggesting the indirect induction of inflammatory response via cytokines. Nevertheless, in a transgenic mouse model of measles virus encephalitis, neuronal expression of CXCL10 was associated with T-cell recruitment, suggesting that neurons may play a role in the induction of immune responses to viral invasion [35] . In recent study Lo et al. showed that NiV infection could induce production of CXCL10 and several other inflammatory chemokines in microvascular, but not in macrovascular endothelial cells [21] . However, in contrast to our study, they cultured endothelial cells in the presence of hydrocortisone, known to have important antiinflammatory activity and to reduce the expression of proinflammatory cytokines [36] , which could account to the differences with our results. In accord to our results, NiV was shown to induce CXCL10 expression as well as several other inflammatory chemokines in brain and lungs of NiV infected hamsters [37] suggesting altogether that the other cytokines may contribute to the CXCL10 proinflammatory effect. CXCL10 has been detected in the cerebrospinal fluid of individuals with HIV-1 infection [38, 39] and in the brains of individuals with HIV-associated dementia [33] , but was absent in uninfected control individuals. These authors also reported that CXCL10 levels were closely associated with the progression of HIV-1-related CNS infection and neuropsychiatric impairment. Moreover, CXCL10 and its receptor CXCR3 were shown to be present in the brains of macaques with SIV/SHIV-E [40, 41] and to elicit apoptosis in fetal neurons [9, 42] . The mechanisms of neuronal injury mediated by the CXCL10 was suggested to be associated to calcium dysregulation during CXCL10 mediated apoptosis [10] , and we hypothesize that overexpression of CXCL10 in Nipah-infected patients may be directly involved in NiV-induced neuropathology. Lack of the appropriate regaents for hamster animal model prevented us from further in vivo analysis of the role of CXCL10 during Nipah infection.