Hotta Kozue, Bazartseren Boldbarrtar, Kaku Yoshihiro, Noguchi Akira, Okutani Akiko, Inoue Satoshi, Yamada Akio
Department of Veterinary Science, National Institute of Infectious Diseases, 162-8640 Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan.
Virus Res. 2009 Jan;139(1):85-90. doi: 10.1016/j.virusres.2008.10.009. Epub 2008 Nov 28.
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.
尽管有几篇关于狂犬病病毒（RABV）受体候选物的报道，但这些受体候选物在决定RABV高度嗜神经性方面所起的可能作用尚未得到充分了解。由于据报道这些RABV候选受体经常与以脂筏和小窝结构为特征的富含胆固醇的微区相关联，我们试图确定由胆固醇耗竭引起的微区扰动是否对RABV感染有任何影响。当用甲基-β-环糊精（MBCD）处理使细胞胆固醇耗竭时，在BHK-21和HEp-2细胞中均观察到RABV吸附和感染增加，但不是增殖而是抑制。MBCD处理对RABV感染产生的这些影响可通过胆固醇重构逆转。这些结果表明，RABV通过位于富含胆固醇的微区以外的入口进入BHK-21或HEp-2细胞，并增加了RABV使用不同机制进入非神经元细胞的可能性。
