Leavitt R, Schlesinger S, Kornfeld S
J Virol. 1977 Jan;21(1):375-85. doi: 10.1128/JVI.21.1.375-385.1977.
Tunicamycin (TM), an antibiotic that inhibits the formation of N-acetylglucosamine-lipid intermediates, thereby preventing the glycosylation of newly synthesized glycoproteins, inhibits the growth of Sindbis virus and vesicular stomatitis virus in BHK cells. At 0.5 mug of TM per ml, the replication of both viruses is inhibited 99.9%. Noninfectious particles were not detected. All the viral proteins were synthesized in the presence of TM, but the glycoproteins were selectively altered in that they migrated faster than normal viral glycoproteins when analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, suggesting defective glycosylation. Within 1 h after TM addition, [14C]glucosamine incorporation into glycoproteins was inhibited 20%, whereas [35S]methionine incorporation was unaffected. By 2 to 3 h after TM addition, glucosamine incorporation had fallen to 15% of control value, with methionine incorporation being 60% of normal. TM did not affect the growth of the nomenveloped encephalomyocarditis virus in BHK cells, demonstrating that TM is not a general inhibitor of protein synthesis. These data demonstrate that TM specifically inhibits the glycosylation of viral glycoproteins and that glycosylation may be essential for the normal assembly of enveloped viral particles.
衣霉素（TM）是一种抗生素，可抑制N - 乙酰葡糖胺 - 脂质中间体的形成，从而阻止新合成糖蛋白的糖基化，它能抑制辛德毕斯病毒和水疱性口炎病毒在BHK细胞中的生长。每毫升含0.5微克TM时，两种病毒的复制均被抑制99.9%。未检测到非感染性颗粒。所有病毒蛋白在TM存在的情况下均可合成，但糖蛋白有选择性地发生了改变，即当通过十二烷基硫酸钠 - 聚丙烯酰胺凝胶电泳分析时，它们的迁移速度比正常病毒糖蛋白快，这表明糖基化存在缺陷。添加TM后1小时内，[14C]葡糖胺掺入糖蛋白的过程被抑制了20%，而[35S]甲硫氨酸的掺入未受影响。添加TM后2至3小时，葡糖胺掺入量降至对照值的15%，甲硫氨酸掺入量为正常水平的60%。TM不影响无包膜的脑心肌炎病毒在BHK细胞中的生长，这表明TM不是蛋白质合成的一般抑制剂。这些数据表明，TM特异性抑制病毒糖蛋白的糖基化，并且糖基化对于包膜病毒颗粒的正常组装可能至关重要。
