Ulferts Rachel, de Boer S Matthijn, van der Linden Lonneke, Bauer Lisa, Lyoo Hey Rhyoung, Maté Maria J, Lichière Julie, Canard Bruno, Lelieveld Daphne, Omta Wienand, Egan David, Coutard Bruno, van Kuppeveld Frank J M
Department of Infectious Diseases and Immunology, Virology Division, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.
Department of Medical Microbiology, Academic Medical Center, Amsterdam, The Netherlands.
Antimicrob Agents Chemother. 2016 Apr 22;60(5):2627-38. doi: 10.1128/AAC.02182-15. Print 2016 May.
Enteroviruses (EVs) represent many important pathogens of humans. Unfortunately, no antiviral compounds currently exist to treat infections with these viruses. We screened the Prestwick Chemical Library, a library of approved drugs, for inhibitors of coxsackievirus B3, identified pirlindole as a potent novel inhibitor, and confirmed the inhibitory action of dibucaine, zuclopenthixol, fluoxetine, and formoterol. Upon testing of viruses of several EV species, we found that dibucaine and pirlindole inhibited EV-B and EV-D and that dibucaine also inhibited EV-A, but none of them inhibited EV-C or rhinoviruses (RVs). In contrast, formoterol inhibited all enteroviruses and rhinoviruses tested. All compounds acted through the inhibition of genome replication. Mutations in the coding sequence of the coxsackievirus B3 (CV-B3) 2C protein conferred resistance to dibucaine, pirlindole, and zuclopenthixol but not formoterol, suggesting that 2C is the target for this set of compounds. Importantly, dibucaine bound to CV-B3 protein 2C in vitro, whereas binding to a 2C protein carrying the resistance mutations was reduced, providing an explanation for how resistance is acquired.
肠道病毒(EVs)是人类许多重要的病原体。不幸的是,目前尚无抗病毒化合物可用于治疗这些病毒感染。我们在已批准药物库Prestwick化学文库中筛选了柯萨奇病毒B3的抑制剂,确定匹吲哚为一种有效的新型抑制剂,并证实了丁卡因、氯氮平、氟西汀和福莫特罗的抑制作用。在对几种肠道病毒属的病毒进行测试时,我们发现丁卡因和匹吲哚抑制B组和D组肠道病毒,丁卡因还抑制A组肠道病毒,但它们均不抑制C组肠道病毒或鼻病毒(RVs)。相比之下,福莫特罗抑制所有测试的肠道病毒和鼻病毒。所有化合物均通过抑制基因组复制发挥作用。柯萨奇病毒B3(CV-B3)2C蛋白编码序列中的突变赋予了对丁卡因、匹吲哚和氯氮平的抗性,但对福莫特罗不产生抗性,这表明2C是这组化合物的作用靶点。重要的是,丁卡因在体外与CV-B3蛋白2C结合,而与携带抗性突变的2C蛋白的结合减少,这为获得抗性的方式提供了解释。