Gibson R, Leavitt R, Kornfeld S, Schlesinger S
Cell. 1978 Apr;13(4):671-9. doi: 10.1016/0092-8674(78)90217-9.
The replication of vesicular stomatitis virus (VSV) is inhibited by tunicamycin (TM), an antibiotic that blocks the formation of N-acetylglucosaminelipid intermediates. We had shown previously that the viral glycoprotein (G) synthesized in cells treated with TM is not glycosylated and is not found on the outer surface of the cell plasma membrane. In this report, we shown that cells exposed to TM produce a low yield of infectious particles. The yield is increased when the temperature during infection is lowered from 37 to 30 degrees C. At 30 degrees C in the presence of TM, both wild-type VSV and the temperature-sensitive mutant ts045 produce particles that do not bind to concanavalin A Sepharose and contain only the nonglycosylated form of G. These particles have a specific infectivity (pfu/cpm) comparable to that of VSV containing glycosylated G.
衣霉素（TM）可抑制水泡性口炎病毒（VSV）的复制，衣霉素是一种能阻断N-乙酰葡糖胺脂质中间体形成的抗生素。我们之前已表明，在用TM处理的细胞中合成的病毒糖蛋白（G）未被糖基化，且未在细胞质膜外表面发现。在本报告中，我们表明暴露于TM的细胞产生的感染性颗粒产量较低。当感染期间的温度从37℃降至30℃时，产量会增加。在30℃且存在TM的情况下，野生型VSV和温度敏感突变体ts045都会产生不与伴刀豆球蛋白A琼脂糖结合且仅含有非糖基化形式G的颗粒。这些颗粒的比感染性（pfu/cpm）与含有糖基化G的VSV相当。
