Crawford G R, Wright P J
J Gen Virol. 1987 Feb;68 ( Pt 2):365-76. doi: 10.1099/0022-1317-68-2-365.
Vero cells were infected by Kunjin virus and radiolabelled in the presence of the leucine analogue, threo-beta-hydroxy-DL-leucine (THL). This analogue is known to prevent preprotein processing in cell-free systems when incorporated into signal peptides. Novel Kunjin virus-specified proteins were detected, namely gp140, p120 and gp92; the designations for the proteins indicate their approximate Mr X 10(-3) and whether they are glycosylated. The glycoproteins gp140 and gp92 were observed in cells labelled with [3H]mannose and bound to concanavalin A. Limited proteolytic digestion of gp140, gp92 and gp66 (related to the envelope protein E), and tryptic peptide mapping of these three glycoproteins and p120 indicated that all four were closely related. The glycoproteins gp140 and gp92 were also detected in cells infected by West Nile virus radiolabelled in the presence of THL. Other effects of THL in Kunjin virus-infected cells were a reduction in the incorporation of radioactive amino acids or mannose, a decrease in the yield of haemagglutinin and infectious virus, an inhibition of processing of gp66 to gp53 and an apparent inhibition of synthesis of P98 and P71. We suggest possible explanations for the THL-induced changes in infected cells based on recent models proposed for the synthesis of the yellow fever and West Nile viral proteins.
将Vero细胞用库京病毒感染,并在亮氨酸类似物苏型-β-羟基-DL-亮氨酸(THL)存在的情况下进行放射性标记。已知这种类似物在掺入信号肽时可防止无细胞系统中的前体蛋白加工。检测到了新型的库京病毒特异性蛋白,即gp140、p120和gp92;这些蛋白的命名表示其大致的Mr×10⁻³以及它们是否被糖基化。在用[³H]甘露糖标记并与伴刀豆球蛋白A结合的细胞中观察到了糖蛋白gp140和gp92。对gp140、gp92和gp66(与包膜蛋白E相关)进行有限的蛋白水解消化,以及对这三种糖蛋白和p120进行胰蛋白酶肽图谱分析表明,所有这四种蛋白密切相关。在用THL进行放射性标记的情况下,在感染西尼罗河病毒的细胞中也检测到了糖蛋白gp140和gp92。THL对感染库京病毒的细胞的其他影响包括放射性氨基酸或甘露糖掺入减少、血凝素和感染性病毒产量降低、gp66加工成gp53受到抑制以及P98和P71合成明显受到抑制。我们根据最近提出的黄热病和西尼罗河病毒蛋白合成模型,对THL诱导的感染细胞变化提出了可能的解释。