Wang Yizhuo, Li Guiming, Yuan Shilin, Gao Qianqian, Lan Ke, Altmeyer Ralf, Zou Gang
Pathogen Diagnostic Center, Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Pathogen Diagnostic Center, Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China School of Life Sciences, Shanghai University, Shanghai, China.
Antimicrob Agents Chemother. 2016 Aug 22;60(9):5357-67. doi: 10.1128/AAC.01073-16. Print 2016 Sep.
Enterovirus 71 (EV-A71) is a major causative pathogen of hand, foot, and mouth disease (HFMD) epidemics. No antiviral therapies are currently available for treating EV-A71 infections. Here, we selected five reported enterovirus inhibitors (suramin, itraconazole [ITZ], GW5074, rupintrivir, and favipiravir) with different mechanisms of action to test their abilities to inhibit EV-A71 replication alone and in combination. All selected compounds have anti-EV-A71 activities in cell culture. The combination of rupintrivir and ITZ or favipiravir was synergistic, while the combination of rupintrivir and suramin was additive. The combination of suramin and favipiravir exerted a strong synergistic antiviral effect. The observed synergy was not due to cytotoxicity, as there was no significant increase in cytotoxicity when compounds were used in combinations at the tested doses. To investigate the potential inhibitory mechanism of favipiravir against enterovirus, two favipiravir-resistant EV-A71 variants were independently selected, and both of them carried an S121N mutation in the finger subdomain of the 3D polymerase. Reverse engineering of this 3D S121N mutation into an infectious clone of EV-A71 confirmed the resistant phenotype. Moreover, viruses resistant to ITZ or favipiravir remained susceptible to other inhibitors. Most notably, combined with ITZ, rupintrivir prevented the development of ITZ-resistant variants. Taken together, these results provide a rational basis for the design of combination regimens for use in the treatment of EV-A71 infections.
肠道病毒71型(EV - A71)是手足口病(HFMD)流行的主要致病病原体。目前尚无抗病毒疗法可用于治疗EV - A71感染。在此,我们选择了五种已报道的具有不同作用机制的肠道病毒抑制剂(苏拉明、伊曲康唑[ITZ]、GW5074、鲁比尼韦和法匹拉韦),以测试它们单独及联合抑制EV - A71复制的能力。所有选定的化合物在细胞培养中均具有抗EV - A71活性。鲁比尼韦与ITZ或法匹拉韦联合具有协同作用,而鲁比尼韦与苏拉明联合具有相加作用。苏拉明与法匹拉韦联合发挥了强大的协同抗病毒作用。观察到的协同作用并非由于细胞毒性,因为在测试剂量下联合使用化合物时细胞毒性没有显著增加。为了研究法匹拉韦对肠道病毒的潜在抑制机制,独立筛选出两个对法匹拉韦耐药的EV - A71变体,它们在3D聚合酶的指状亚结构域均携带S121N突变。将此3D S121N突变反向工程导入EV - A71感染性克隆证实了耐药表型。此外,对ITZ或法匹拉韦耐药的病毒对其他抑制剂仍敏感。最值得注意的是,鲁比尼韦与ITZ联合可防止ITZ耐药变体的产生。综上所述,这些结果为设计用于治疗EV - A71感染的联合治疗方案提供了合理依据。