Talbot P J, Vance D E
Can J Biochem. 1980 Oct;58(10):1131-7. doi: 10.1139/o80-151.
Chloroquine and NH4Cl, potent inhibitors of lysosomal function, decreased the production of infectious Sindbis virus particles in BHK-21 cells by 10- and 12-fold, respectively. There were no apparent toxic effects on cells exposed to these lysosomotropic agents. These chemicals did not alter the rate of cellular protein synthesis, with the exception of a reversible twofold inhibition by chloroquine. No additive effects of chloroquine and NH4Cl were observed when the cells were saturated with these weak bases, which suggests that their effect is exerted via the same mechanism, most likely as a result of an increase in lysosomal pH. The reduction in the formation of Sindbis virions was monitored by incorporation of [35S]methionine and shown to be fourfold by chloroquine or NH4Cl at 5 h postinfection but negligible at 11 h postinfection. These results strongly suggest that a productive Sindbis virus infection requires functional lysosomes. Thus, endocytosis is probably the main infectious mechanism for penetration of this virus into BHK-21 cells.
氯喹和氯化铵是溶酶体功能的强效抑制剂，它们分别使BHK - 21细胞中传染性辛德毕斯病毒颗粒的产生减少了10倍和12倍。对暴露于这些溶酶体促渗剂的细胞没有明显的毒性作用。这些化学物质除了氯喹有可逆的两倍抑制作用外，并没有改变细胞蛋白质合成的速率。当细胞被这些弱碱饱和时，未观察到氯喹和氯化铵的相加效应，这表明它们的作用是通过相同的机制发挥的，很可能是溶酶体pH值升高的结果。通过掺入[35S]甲硫氨酸监测辛德毕斯病毒粒子形成的减少情况，结果显示在感染后5小时，氯喹或氯化铵可使其减少四倍，但在感染后11小时可忽略不计。这些结果有力地表明，辛德毕斯病毒的有效感染需要功能性溶酶体。因此，内吞作用可能是该病毒进入BHK - 21细胞的主要感染机制。
