Adams R H, Brown D T
J Virol. 1982 Feb;41(2):692-702. doi: 10.1128/JVI.41.2.692-702.1982.
Brief treatment of Sindbis virus-infected BHK-21 or Vero cells with low concentrations of trypsin irreversibly blocked further production of progeny virions after removal of the enzyme. The inhibitory effects of the trypsin treatment could only be demonstrated in cells in which virus infection was established; optimal inhibition occurred at ca. 3 h postinfection. Production of virus structural proteins PE2, E1, and C occurred at normal levels in inhibited cells. PE2 and E1 were also transported to the cell plasma membrane during inhibition; however, PE2 was not cleaved to E2, and little capsid protein became membrane associated relative to control cells. Although trypsin treatment had no effect on Sindbis protein synthesis, the production of both 26S and 42S RNA was greatly reduced. Similar trypsin treatment of BHK cells infected with vesicular stomatitis virus had no detectable effect on the course of virus infection.
用低浓度胰蛋白酶对辛德毕斯病毒感染的BHK - 21或Vero细胞进行短暂处理后,去除该酶会不可逆地阻断子代病毒粒子的进一步产生。胰蛋白酶处理的抑制作用仅在已建立病毒感染的细胞中得到证实;最佳抑制发生在感染后约3小时。在受抑制的细胞中,病毒结构蛋白PE2、E1和C的产生水平正常。在抑制过程中,PE2和E1也被转运到细胞质膜;然而,PE2没有裂解为E2,并且相对于对照细胞,很少有衣壳蛋白与膜结合。尽管胰蛋白酶处理对辛德毕斯病毒蛋白合成没有影响,但26S和42S RNA的产生都大大减少。用类似的胰蛋白酶处理感染水疱性口炎病毒的BHK细胞,对病毒感染进程没有可检测到的影响。