Christopher S. Bond Life Sciences Center, Department of Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia, Missouri, USA.
Antimicrob Agents Chemother. 2012 Sep;56(9):4718-28. doi: 10.1128/AAC.00957-12. Epub 2012 Jun 25.
Severe acute respiratory syndrome (SARS) is a highly contagious disease, caused by SARS coronavirus (SARS-CoV), for which there are no approved treatments. We report the discovery of a potent inhibitor of SARS-CoV that blocks replication by inhibiting the unwinding activity of the SARS-CoV helicase (nsp13). We used a Förster resonance energy transfer (FRET)-based helicase assay to screen the Maybridge Hitfinder chemical library. We identified and validated a compound (SSYA10-001) that specifically blocks the double-stranded RNA (dsRNA) and dsDNA unwinding activities of nsp13, with 50% inhibitory concentrations (IC(50)s) of 5.70 and 5.30 μM, respectively. This compound also has inhibitory activity (50% effective concentration [EC(50)] = 8.95 μM) in a SARS-CoV replicon assay, with low cytotoxicity (50% cytotoxic concentration [CC(50)] = >250 μM), suggesting that the helicase plays a still unidentified critical role in the SARS-CoV life cycle. Enzyme kinetic studies on the mechanism of nsp13 inhibition revealed that SSYA10-001 acts as a noncompetitive inhibitor of nsp13 with respect to nucleic acid and ATP substrates. Moreover, SSYA10-001 does not affect ATP hydrolysis or nsp13 binding to the nucleic acid substrate. SSYA10-001 did not inhibit hepatitis C virus (HCV) helicase, other bacterial and viral RNA-dependent RNA polymerases, or reverse transcriptase. These results suggest that SSYA10-001 specifically blocks nsp13 through a novel mechanism and is less likely to interfere with the functions of cellular enzymes that process nucleic acids or ATP. Hence, it is possible that SSYA10-001 inhibits unwinding by nsp13 by affecting conformational changes during the course of the reaction or translocation on the nucleic acid. SSYA10-001 will be a valuable tool for studying the specific role of nsp13 in the SARS-CoV life cycle, which could be a model for other nidoviruses and also a candidate for further development as a SARS antiviral target.
严重急性呼吸系统综合症(SARS)是一种高传染性疾病,由 SARS 冠状病毒(SARS-CoV)引起,目前尚无批准的治疗方法。我们报告了一种有效的 SARS-CoV 抑制剂的发现,该抑制剂通过抑制 SARS-CoV 解旋酶(nsp13)的解旋活性来阻止复制。我们使用基于荧光共振能量转移(FRET)的解旋酶测定法筛选了 Maybridge Hitfinder 化学文库。我们鉴定并验证了一种化合物(SSYA10-001),它可以特异性地阻断 nsp13 的双链 RNA(dsRNA)和 dsDNA 解旋活性,其 50%抑制浓度(IC50)分别为 5.70 和 5.30 μM。该化合物在 SARS-CoV 复制子测定中也具有抑制活性(50%有效浓度[EC50] = 8.95 μM),细胞毒性低(50%细胞毒性浓度[CC50]>250 μM),这表明解旋酶在 SARS-CoV 生命周期中仍发挥着尚未确定的关键作用。关于 nsp13 抑制机制的酶动力学研究表明,SSYA10-001 是 nsp13 的非竞争性抑制剂,针对核酸和 ATP 底物。此外,SSYA10-001 不影响 ATP 水解或 nsp13 与核酸底物的结合。SSYA10-001 不抑制丙型肝炎病毒(HCV)解旋酶、其他细菌和病毒 RNA 依赖性 RNA 聚合酶或逆转录酶。这些结果表明,SSYA10-001 通过一种新的机制特异性地阻断 nsp13,不太可能干扰参与核酸或 ATP 加工的细胞酶的功能。因此,SSYA10-001 可能通过影响反应过程中的构象变化或在核酸上的易位来抑制 nsp13 的解旋。SSYA10-001 将成为研究 nsp13 在 SARS-CoV 生命周期中特定作用的有价值的工具,它可以作为其他 nidoviruses 的模型,也可以作为进一步开发 SARS 抗病毒靶标的候选药物。