CXCL10 is the substrate for serine protease CD26/dipeptidylpeptidase 4, which cleaves its aminoterminal part and alters its receptor binding and signaling, producing therefore an antagonistic protein with dominant negative function [43] . This antagonist form of CXCL10 was very recently shown to play an important role in patients chronically infected with hepatitis C virus [44] and to present an important negative prognostic marker for the response to therapy [45, 46] . Whether this cleaved antagonist form of CXCL10 is generated during NiV-infection remains to be elucidated. If produced, its action on inhibition of the physiological role of CXCL10, may play an important role in the pathogenesis of NiV-encephalitis.