Zhao Qi, Li Shuang, Xue Fei, Zou Yilong, Chen Cheng, Bartlam Mark, Rao Zihe
Tsinghua-Nankai-IBP Joint Research Group for Structural Biology, Tsinghua University, Beijing, China.
J Virol. 2008 Sep;82(17):8647-55. doi: 10.1128/JVI.00298-08. Epub 2008 Jun 18.
The newly emergent human coronavirus HKU1 (HCoV-HKU1) was first identified in Hong Kong in 2005. Infection by HCoV-HKU1 occurs worldwide and causes syndromes such as the common cold, bronchitis, and pneumonia. The CoV main protease (M(pro)), which is a key enzyme in viral replication via the proteolytic processing of the replicase polyproteins, has been recognized as an attractive target for rational drug design. In this study, we report the structure of HCoV-HKU1 M(pro) in complex with a Michael acceptor, inhibitor N3. The structure of HCoV-HKU1 provides a high-quality model for group 2A CoVs, which are distinct from group 2B CoVs such as severe acute respiratory syndrome CoV. The structure, together with activity assays, supports the relative conservation at the P1 position that was discovered by sequencing the HCoV-HKU1 genome. Combined with structural data from other CoV M(pro)s, the HCoV-HKU1 M(pro) structure reported here provides insights into both substrate preference and the design of antivirals targeting CoVs.
新出现的人类冠状病毒HKU1(HCoV-HKU1)于2005年首次在香港被发现。HCoV-HKU1的感染在全球范围内发生,并引起诸如普通感冒、支气管炎和肺炎等综合征。冠状病毒主要蛋白酶(M(pro))是通过对复制酶多聚蛋白进行蛋白水解加工从而在病毒复制中起关键作用的一种酶,已被认为是合理药物设计的一个有吸引力的靶点。在本研究中,我们报道了HCoV-HKU1 M(pro)与迈克尔受体抑制剂N3结合的结构。HCoV-HKU1的结构为2A组冠状病毒提供了一个高质量模型,2A组冠状病毒与严重急性呼吸综合征冠状病毒等2B组冠状病毒不同。该结构与活性测定结果一起,支持了通过对HCoV-HKU1基因组测序所发现的P1位置的相对保守性。结合来自其他冠状病毒M(pro)的结构数据,本文报道的HCoV-HKU1 M(pro)结构为底物偏好性以及针对冠状病毒的抗病毒药物设计提供了见解。