Institute of Medical Virology, University of Zurich, 8057 Zurich, Switzerland.
Immunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California 92037, United States.
ACS Infect Dis. 2022 Jul 8;8(7):1265-1279. doi: 10.1021/acsinfecdis.2c00008. Epub 2022 Jun 29.
There is a pressing need for host-directed therapeutics that elicit broad-spectrum antiviral activities to potentially address current and future viral pandemics. Apratoxin S4 (Apra S4) is a potent Sec61 inhibitor that prevents cotranslational translocation of secretory proteins into the endoplasmic reticulum (ER), leading to anticancer and antiangiogenic activity both in vitro and in vivo. Since Sec61 has been shown to be an essential host factor for viral proteostasis, we tested Apra S4 in cellular models of viral infection, including SARS-CoV-2, influenza A virus, and flaviviruses (Zika, West Nile, and Dengue virus). Apra S4 inhibited viral replication in a concentration-dependent manner and had high potency particularly against SARS-CoV-2 and influenza A virus, with subnanomolar activity in human cells. Characterization studies focused on SARS-CoV-2 revealed that Apra S4 impacted a post-entry stage of the viral life-cycle. Transmission electron microscopy revealed that Apra S4 blocked formation of stacked double-membrane vesicles, the sites of viral replication. Apra S4 reduced dsRNA formation and prevented viral protein production and trafficking of secretory proteins, especially the spike protein. Given the potent and broad-spectrum activity of Apra S4, further preclinical evaluation of Apra S4 and other Sec61 inhibitors as antivirals is warranted.
目前迫切需要宿主定向治疗药物,以产生广谱抗病毒活性,从而有可能应对当前和未来的病毒大流行。Apratoxin S4(Apra S4)是一种有效的 Sec61 抑制剂,可防止分泌蛋白在共翻译过程中易位到内质网(ER),从而在体外和体内均具有抗癌和抗血管生成活性。由于 Sec61 已被证明是病毒蛋白稳态的必需宿主因子,因此我们在病毒感染的细胞模型中测试了 Apra S4,包括 SARS-CoV-2、甲型流感病毒和黄病毒(寨卡病毒、西尼罗河病毒和登革热病毒)。Apra S4 以浓度依赖性方式抑制病毒复制,对 SARS-CoV-2 和甲型流感病毒具有很高的效力,在人细胞中的活性达到亚纳摩尔级。针对 SARS-CoV-2 的特征研究表明,Apra S4 影响了病毒生命周期的进入后阶段。透射电子显微镜显示,Apra S4 阻断了堆叠双层膜泡的形成,这是病毒复制的部位。Apra S4 减少了 dsRNA 的形成,并阻止了病毒蛋白的产生和分泌蛋白的运输,尤其是刺突蛋白。鉴于 Apra S4 的强大和广谱活性,有必要进一步对 Apra S4 和其他 Sec61 抑制剂作为抗病毒药物进行临床前评估。