Effect of cellular cholesterol depletion on rabies virus infection
Effect of cellular cholesterol depletion on rabies virus infection
复制标题
DOI：
10.1016/j.virusres.2008.10.009
复制
发表时间：
2009-01-01
期刊：
影响因子：
5
通讯作者：
Yamada, Akio
中科院分区：
文献类型：
--
作者：
Hotta, Kozue;Bazartseren, Boldbarrtar;Yamada, Akio
虽然有一些关于狂犬病病毒（RABV）受体候选者的报道，但这些受体候选者在确定RABV的高度嗜神经性方面可能发挥的作用尚未得到很好的理解。由于这些候选受体的RABV被报道经常与富含胆固醇的微区脂筏和小窝结构的特点，我们试图确定是否由胆固醇消耗引起的微区的干扰显示任何影响RABV感染。当细胞胆固醇被甲基-β-环糊精（MBCD）处理耗尽时，在BHK-21和HEp-2细胞中观察到RABV吸附和感染增加，但不是增殖而是抑制。MBCD对RABV感染的这些作用可被胆固醇重建逆转。这些结果表明，RABV进入BHK-21或HEp-2细胞通过进入端口以外的那些位于富含胆固醇的微域，并提高了RABV使用不同的机制进入非神经元细胞的可能性。皇冠版权所有（C）2008年出版的爱思唯尔B. V.保留所有权利。
Although there are several reports on candidates for rabies virus (RABV) receptor, possible roles played by these receptor candidates in determination of highly neurotropic nature of RABV have not been well understood. Since these candidate receptors for RABV were reported to be frequently associated with cholesterol-rich microdomains characterized by lipid rafts and caveolae structures, we attempted to determine whether the disturbance of microdomains caused by the cholesterol depletion showed any effects on RABV infection. When the cellular cholesterol was depleted by methyl-beta-cyclodextrin (MBCD) treatment, increase in RABV adsorption and infection, but not multiplication rather than suppression was observed in both BHK-21 and HEp-2 cells. These effects exerted by MBCD treatment on RABV infection could be reversed by cholesterol reconstitution. These results suggest that RABV enters BHK-21 or HEp-2 cells through ports of entry other than those located on cholesterol-rich microdomains and raise the possibility that RABV uses different mechanisms to enter the non-neuronal cells. Crown Copyright (C) 2008 Published by Elsevier B.V. All rights reserved.