肽
血管紧张素转化酶2
病毒进入
血浆蛋白结合
小分子
生物
严重急性呼吸综合征冠状病毒2型(SARS-CoV-2)
体外
化学
生物化学
配体(生物化学)
2019年冠状病毒病(COVID-19)
细胞生物学
病毒学
病毒
受体
病毒复制
医学
疾病
病理
传染病(医学专业)
作者
Max J. Bedding,Charlotte Franck,Jason Johansen‐Leete,Anupriya Aggarwal,Joshua W. C. Maxwell,Karishma Patel,Paige M. E. Hawkins,Jason K. K. Low,Rezwan Siddiquee,Hakimeh Moghaddas Sani,Daniel Ford,Stuart Turville,Joel P. Mackay,Toby Passioura,Mary Christie,Richard J. Payne
标识
DOI:10.1021/acschembio.3c00568
摘要
The development of effective antiviral compounds is essential for mitigating the effects of the COVID-19 pandemic. Entry of SARS-CoV-2 virions into host cells is mediated by the interaction between the viral spike (S) protein and membrane-bound angiotensin-converting enzyme 2 (ACE2) on the surface of epithelial cells. Inhibition of this viral protein-host protein interaction is an attractive avenue for the development of antiviral molecules with numerous spike-binding molecules generated to date. Herein, we describe an alternative approach to inhibit the spike-ACE2 interaction by targeting the spike-binding interface of human ACE2 via mRNA display. Two consecutive display selections were performed to direct cyclic peptide ligand binding toward the spike binding interface of ACE2. Through this process, potent cyclic peptide binders of human ACE2 (with affinities in the picomolar to nanomolar range) were identified, two of which neutralized SARS-CoV-2 entry. This work demonstrates the potential of targeting ACE2 for the generation of anti-SARS-CoV-2 therapeutics as well as broad spectrum antivirals for the treatment of SARS-like betacoronavirus infection.
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