A hantavirus causing hemorrhagic fever with renal syndrome requires gC1qR/p32 for efficient cell binding and infection
A hantavirus causing hemorrhagic fever with renal syndrome requires gC1qR/p32 for efficient cell binding and infection
复制标题
DOI：
10.1016/j.virol.2008.08.035
复制
发表时间：
2008-11-25
期刊：
影响因子：
3.7
通讯作者：
Ahn, Byung-Yoon
中科院分区：
文献类型：
--
作者：
Choi, Yun;Kwon, Young-Chan;Ahn, Byung-Yoon
汉坦病毒（HTNV）是一种引起肾综合征出血热（HFRS）的致病性汉坦病毒。HTNV感染由α v β 3整联蛋白介导。我们使用Vero E6细胞匀浆的蛋白质印迹来证明放射性标记的HTNV病毒粒子与gC 1 qR/p32结合，gC 1 qR/p32是一种酸性32 kDa蛋白，被称为补体C1 q球状头部结构域的受体。RNAi介导的gC 1 qR/p32抑制显著降低人肺上皮A549细胞中HTNV结合和感染。相反，猴或人gC 1 qR/p32的瞬时表达使非允许性CHO细胞对HTNV感染敏感。这些结果表明gC 1 qR/p32在HTNV感染和发病机制中起重要作用。(C)2008年爱思唯尔公司All rights reserved.
Hantaan virus (HTNV) is a pathogenic hantavirus that causes hemorrhagic fever with renal syndrome (HFRS). HTNV infection is mediated by alpha v beta 3 integrin. We used protein blots of Vero E6 cell homogenates to demonstrate that radiolabeled HTNV virions bind to gC1qR/p32, the acidic 32-kDa protein known as the receptor for the globular head domain of complement C1q. RNAi-mediated suppression of gC1qR/p32 markedly reduced HTNV binding and infection in human lung epithelial A549 cells. Conversely, transient expression of either simian or human gC1qR/p32 rendered non-permissive CHO cells susceptible to HTNV infection. These results suggest an important role for gC1qR/p32 in HTNV infection and pathogenesis. (C) 2008 Elsevier Inc. All rights reserved.