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Different chemokine expression in lethal and non‐lethal murine west nile virus infection
Author(s) -
Shirato Kazuya,
Kimura Takashi,
Mizutani Tetsuya,
Kariwa Hiroaki,
Takashima Ikuo
Publication year - 2004
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20205
Subject(s) - virology , biology , chemokine , virus , flavivirus , cxcl13 , japanese encephalitis , ccl5 , cxcl10 , encephalitis , immunology , chemokine receptor , t cell , immune system , il 2 receptor
West Nile (WN) virus is a mosquito‐borne flavivirus that can cause lethal encephalitis in humans and horses. The WN virus endemic in New York City (NY) in 1999 caused large‐scale mortality of wild birds that was not evident in endemic areas in other parts of the world, and the pathogenesis of the WN virus strain isolated in NY (NY strain) appears to differ from that of previously isolated strains. However, the pathogenesis of NY strain infection remains unclear. This study examined CC (RANTES/CCL5, MIP‐1α/CCL3, MIP‐1β/CCL4) and CXC (IP‐10/CXCL10, B lymphocyte chemoattractant (BLC/CXCL13), and B cell‐ and monocyte‐activating chemokine (BMAC/CXCL14)) chemokine expression during lethal NY strain and non‐lethal Eg101 strain infection in mice. We found that the mRNA of the CC chemokines, RANTES, MIP‐1α, MIP‐1β, and IP‐10 was highly up‐regulated in the brain of NY strain‐infected mice. By contrast, BLC mRNA was not detected in either group of mice, and BMAC mRNA was highly up‐regulated in late stage of infection with the non‐lethal Eg101 strain relative to levels in NY strain‐infected mice. J. Med. Virol. 74:507–513, 2004. © 2004 Wiley‐Liss, Inc.