Author: Mathieu, Cyrille; Guillaume, Vanessa; Sabine, Amélie; Ong, Kien Chai; Wong, Kum Thong; Legras-Lachuer, Catherine; Horvat, Branka
Title: Lethal Nipah Virus Infection Induces Rapid Overexpression of CXCL10 Document date: 2012_2_29
ID: 0d3vy87b_17
Snippet: 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 respon.....
Document: 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.
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