Richardson C D, Vance D E
J Biol Chem. 1978 Jul 10;253(13):4584-9.
The effect of colchicine, Nocodazole, and dibucaine on the assembly of Semliki Forest virus was investigated. Colchicine, Nocodazole, and dibucaine reduced the production of extracellular virus by 75 to 90%. Lumicolchicine had no effect on virus growth. Other control experiments showed no effect by these drugs on the incorporation of [3H]leucine into material precipitated by trichloroacetic acid. Colchicine (100 micron) disrupted the microtubles of the baby hamster kidney cells (BHK-21), whereas dibucaine did not alter microtubule polymerization. The stage of virus assembly inhibited by colchicine and dibucaine was studied by experiments with [3H]-leucine or [35S]methionine. At various times after addition of one of these drugs, the incorporation of the labeled precursors into viral proteins associated with fractions enriched for endoplasmic reticulum or plasma membrane from the cell was evaluated. The results clearly show that the envelope and nucleocapsid proteins of the virus move to the plasma membrane of the cell where they accumulate. The studies strongly suggest that the cytoskeletal system is involved in the final stages of morphogenesis of Semliki Forest virus from the plasma membrane.
研究了秋水仙碱、诺考达唑和丁卡因对辛德毕斯病毒装配的影响。秋水仙碱、诺考达唑和丁卡因使细胞外病毒产量降低了75%至90%。光秋水仙碱对病毒生长没有影响。其他对照实验表明，这些药物对[3H]亮氨酸掺入三氯乙酸沉淀的物质中没有影响。秋水仙碱（100微米）破坏了幼仓鼠肾细胞（BHK-21）的微管，而丁卡因没有改变微管聚合。通过用[3H]亮氨酸或[35S]甲硫氨酸进行实验，研究了秋水仙碱和丁卡因抑制病毒装配的阶段。在添加这些药物之一后的不同时间，评估标记前体掺入与细胞内质网或质膜富集部分相关的病毒蛋白中的情况。结果清楚地表明，病毒的包膜蛋白和核衣壳蛋白移动到细胞的质膜并在那里积累。这些研究强烈表明，细胞骨架系统参与了辛德毕斯病毒从质膜形态发生的最后阶段。
