Inhibitors of COP-mediated transport and cholera toxin action inhibit simian virus 40 infection
Inhibitors of COP-mediated transport and cholera toxin action inhibit simian virus 40 infection
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DOI：
10.1091/mbc.01-12-0592
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发表时间：
2002-05-01
影响因子：
3.3
通讯作者：
Parton, RG
中科院分区：
文献类型：
--
作者：
Richards, AA;Stang, E;Parton, RG
猿猴病毒 40 (SV40) 是一种无包膜病毒，已被证明可以通过一种明显新颖的感染进入途径从表面小窝传播到内质网。我们现在表明，最初的进入步骤被布雷菲德菌素 A 和 20 摄氏度的孵育所阻断。在进入步骤之后，病毒通过未知途径到达粗面内质网的区域。该细胞内运输途径对布雷菲德菌素 A 也敏感。 GTP 限制性 ADP 核糖基化因子 1 (Arf1) 和 Sar1 突变体的表达以及 betaCOP 抗体的显微注射可强烈抑制感染。此外，我们还证明二肽 N-苯甲酰基-氧羰基-Gly-Phe-酰胺可有效抑制 SV40 感染，同时还可抑制霍乱毒素作用的晚期事件。我们的结果确定了 SV40 感染的新型抑制剂，并表明 SV40 需要 COPI 和 COPII 依赖性转运步骤才能成功感染。
Simian virus 40 (SV40) is a nonenveloped virus that has been shown to pass from surface caveolae to the endoplasmic reticulum in an apparently novel infectious entry pathway. We now show that the initial entry step is blocked by brefeldin A and by incubation at 20degreesC. Subsequent to the entry step, the virus reaches a domain of the rough endoplasmic reticulum by an unknown pathway. This intracellular trafficking pathway is also brefeldin A sensitive. Infection is strongly inhibited by expression of GTP-restricted ADP-ribosylation factor 1 (Arf1) and Sar1 mutants and by microinjection of antibodies to betaCOP. In addition, we demonstrate a potent inhibition of SV40 infection by the dipeptide N-benzoyl-oxycarbonyl-Gly-Phe-amide, which also inhibits late events in cholera toxin action. Our results identify novel inhibitors of SV40 infection and show that SV40 requires COPI- and COPII-dependent transport steps for successful infection.