Glasgow et al. (1) report their mutagenesis survey of ACE2 traps for treatment of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The virus invades human cells via host ACE2 receptor, and strategies aimed at disrupting this process are being explored. As compared to monoclonal antibodies and targeted vaccines that are prone to mutational escape of the virus, the ACE2 trap strategy has unique advantages and was shown to be efficacious in experimental and clinical tests (2, 3). Current studies, including Glasgow et al., focus on further improvements through alternative designs. These include extending in vivo half-life with an Fc tag (4, 5), increasing Spike-binding affinity via mutagenesis (1, 6), and inactivating ACE2 peptidase activity (1, 4). The Glasgow study combined all three approaches in their lead design (1 …

中文翻译：

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血管紧张素转换酶 2 (ACE2) 的 His345 突变体对血管紧张素 II 保持酶促活性 [生物科学]

格拉斯哥等。( 1 ) 报告了他们对用于治疗严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 的 ACE2 陷阱的诱变调查。该病毒通过宿主 ACE2 受体侵入人体细胞，目前正在探索旨在破坏这一过程的策略。与容易发生病毒突变逃逸的单克隆抗体和靶向疫苗相比，ACE2 诱捕策略具有独特的优势，并在实验和临床试验中证明是有效的 ( 2 , 3 )。当前的研究，包括 Glasgow 等人，都侧重于通过替代设计进一步改进。这些包括使用 Fc 标签延长体内半衰期 ( 4 , 5 )，通过诱变增加 Spike 结合亲和力 (1 , 6 )，并灭活 ACE2 肽酶活性 ( 1 , 4 )。格拉斯哥的研究在其主要设计中结合了所有三种方法（1 …