Hofmann-Winkler Heike, Gnirß Kerstin, Wrensch Florian, Pöhlmann Stefan
Infection Biology Unit, German Primate Center, Göttingen, Germany.
J Infect Dis. 2015 Oct 1;212 Suppl 2(Suppl 2):S172-80. doi: 10.1093/infdis/jiv101. Epub 2015 Apr 2.
The ongoing Ebola virus (EBOV) disease (EVD) epidemic in Western Africa is the largest EVD outbreak recorded to date and requires the rapid development and deployment of antiviral measures. The viral glycoprotein (GP) facilitates host cell entry and, jointly with cellular interaction partners, constitutes a potential target for antiviral intervention. However, it is unknown whether the GPs of the currently and previously circulating EBOVs use the same mechanisms for cellular entry and are thus susceptible to inhibition by the same antivirals and cellular defenses. Here, we show that the GPs of the EBOVs circulating in 1976 and 2014 transduce the same spectrum of target cells, use the same cellular factors for host cell entry, and are comparably susceptible to blockade by antiviral interferon-induced transmembrane proteins and neutralizing antibody KZ52. Thus, the viruses responsible for the ongoing EVD epidemic should be fully susceptible to established antiviral strategies targeting GP and cellular entry factors.
西非正在爆发的埃博拉病毒(EBOV)病(EVD)疫情是迄今为止有记录以来最大规模的埃博拉病毒病疫情,需要迅速研发并部署抗病毒措施。病毒糖蛋白(GP)促进宿主细胞进入,并与细胞相互作用伙伴共同构成抗病毒干预的潜在靶点。然而,目前和以前流行的埃博拉病毒的糖蛋白是否利用相同的机制进入细胞,因而是否易受相同抗病毒药物和细胞防御机制的抑制,目前尚不清楚。在此,我们表明,1976年和2014年流行的埃博拉病毒的糖蛋白转导相同范围的靶细胞,利用相同的细胞因子进入宿主细胞,并且对抗病毒干扰素诱导的跨膜蛋白和中和抗体KZ52的阻断具有相似的敏感性。因此,导致当前埃博拉病毒病疫情的病毒应该对针对糖蛋白和细胞进入因子的既定抗病毒策略完全敏感。