Shirato Kazuya, Kimura Takashi, Mizutani Tetsuya, Kariwa Hiroaki, Takashima Ikuo
Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.
J Med Virol. 2004 Nov;74(3):507-13. doi: 10.1002/jmv.20205.
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-1 alpha/CCL3, MIP-1 beta/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-1 alpha, MIP-1 beta, 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.
西尼罗河（WN）病毒是一种由蚊子传播的黄病毒，可导致人类和马匹发生致命性脑炎。1999年在纽约市（NY）流行的WN病毒导致野生鸟类大规模死亡，这在世界其他地区的流行地区并不明显，并且在纽约分离出的WN病毒株（NY株）的发病机制似乎与先前分离出的毒株不同。然而，NY株感染的发病机制仍不清楚。本研究检测了致死性NY株和非致死性Eg101株感染小鼠过程中CC趋化因子（调节激活正常T细胞表达和分泌因子/CCL5、巨噬细胞炎症蛋白-1α/CCL3、巨噬细胞炎症蛋白-1β/CCL4）和CXC趋化因子（干扰素诱导蛋白10/CXCL10、B淋巴细胞趋化因子（BLC/CXCL13）以及B细胞和单核细胞激活趋化因子（BMAC/CXCL14））的表达情况。我们发现，在感染NY株的小鼠大脑中，CC趋化因子调节激活正常T细胞表达和分泌因子、巨噬细胞炎症蛋白-1α、巨噬细胞炎症蛋白-1β以及干扰素诱导蛋白10的mRNA高度上调。相比之下，在两组小鼠中均未检测到BLC mRNA，并且相对于感染NY株的小鼠，在感染非致死性Eg101株的后期，BMAC mRNA高度上调。
Zotero 插件