MULTIPLE PROTEASES IN FOOT-AND-MOUTH-DISEASE VIRUS-REPLICATION
MULTIPLE PROTEASES IN FOOT-AND-MOUTH-DISEASE VIRUS-REPLICATION
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DOI：
10.1128/jvi.50.3.878-883.1984
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发表时间：
1984-01-01
影响因子：
5.4
通讯作者：
COLLEN, D
中科院分区：
文献类型：
--
作者：
BURROUGHS, JN;SANGAR, DV;COLLEN, D
口蹄疫病毒RNA在兔网织红细胞裂解物中短时间间隔的翻译导致肽P20 a、P16和P88的产生。如果进一步的翻译被阻止，结构蛋白前体P88不会被切割，即使在长时间的孵育后。显然，P20 a-P16和P88之间以及P88和P52（P2）之间的切割机制不同于产生结构蛋白的二级切割机制。用蛋白酶抑制剂D-缬氨酰苯丙氨酰赖氨酰氯甲基酮处理口蹄疫病毒感染的仓鼠肾BHK-21细胞，阻止了P20 a-P16和P88之间的体内切割，但对任何其他切割事件没有影响。显然，口蹄疫病毒多蛋白的切割利用2种不同的宿主蛋白酶。
Translation of foot-and-mouth disease virus RNA in a rabbit reticulocyte lysate for short time intervals resulted in the production of the peptides P20a, P16 and P88. If further translation was prevented, the structural protein precursor P88 was not cleaved, even after prolonged incubation. Evidently, the mechanism of the cleavage between P20a-P16 and P88 and of that between P88 and P52 (P2) differs from the mechanism of the secondary cleavages which produce the structural proteins. Treatment of foot-and-mouth disease virus-infected hamster kidney BHK-21 cells with the protease inhibitor D-valyl phenylalanyl lysyl chloromethyl ketone prevented the in vivo cleavage between P20a-P16 and P88, but had no effect on any of the other cleavage events. Apparently, the cleavage of the foot-and-mouth disease virus polyprotein utilizes 2 different host proteases.