Nuclear Signalling Laboratory, Department of Biochemistry and Molecular Biology, School of Biomedical Sciences, Monash University, Melbourne, Australia.
National Center for Biodefense and Infectious Diseases, School of Systems Biology, George Mason University, Manassas, VA, USA.
Antiviral Res. 2018 Mar;151:8-19. doi: 10.1016/j.antiviral.2018.01.007. Epub 2018 Jan 11.
Although the alphavirus Venezuelan equine encephalitis virus (VEEV) has been the cause of multiple outbreaks resulting in extensive human and equine mortality and morbidity, there are currently no anti-VEEV therapeutics available. VEEV pathogenicity is largely dependent on targeting of the viral capsid protein (CP) to the host cell nucleus through the nuclear transporting importin (Imp) α/β1 heterodimer. Here we perform a high-throughput screen, combined with nested counterscreens to identify small molecules able to inhibit the Impα/β1:CP interaction for the first time. Several compounds were able to significantly reduce viral replication in infected cells. Compound G281-1564 in particular could inhibit VEEV replication at low μM concentration, while showing minimal toxicity, with steady state and dynamic quantitative microscopic measurements confirming its ability to inhibit CP nuclear import. This study establishes the principle that inhibitors of CP nucleocytoplasmic trafficking can have potent antiviral activity against VEEV, and represents a platform for future development of safe anti-VEEV compounds with high efficacy and specificity.
尽管甲病毒委内瑞拉马脑炎病毒(VEEV)已经引起了多次暴发,导致大量人和马死亡和发病,但目前尚无抗 VEEV 的治疗方法。VEEV 的致病性在很大程度上取决于通过核转运进口蛋白(Imp)α/β1 异二聚体将病毒衣壳蛋白(CP)靶向宿主细胞核。在这里,我们进行了高通量筛选,并结合嵌套的反筛选,首次鉴定出能够抑制 Impα/β1:CP 相互作用的小分子。几种化合物能够显著降低感染细胞中的病毒复制。特别是化合物 G281-1564 能够以低 μM 浓度抑制 VEEV 复制,同时表现出最小的毒性,稳态和动态定量显微镜测量证实其能够抑制 CP 核输入。本研究确立了 CP 核质转运抑制剂对 VEEV 具有强大抗病毒活性的原则,为未来开发高效、特异性的安全抗 VEEV 化合物提供了平台。