Coronavirus and Enzymes: What the Past Told us?

Hortense Ferriz, R. Buchet
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引用次数: 1

Abstract

Novelty always frightens, provoking overreactions. On the other hand, the strategy of viral infection, including that of coronavirus (COVID-19), originates from ancient times and can be summarized, as 1) entry into host cells, 2) interfering with host genetic program to duplicate virus entity; 3) infection into surrounding cells. These are the strengths of the viruses but also their weaknesses since it identifies possible targets to prevent infection. At each step of viral infection, viral enzymatic reactions are observed, which may be similar to those occurring in another closely related family of viruses. COVID-19 is related with 88% to two bat-derived severe acute respiratory syndromes (SARS)-like coronaviruses (bat-SLCoVZC45 and bat-SL-CoVZXC21, collected in 2018 in Zhoushan, eastern China), SARS-CoV (about 79%) and MERS-CoV (about 50%) [1]. The penetration of the COVID-19, similar to that of SARS-CoV, into the infected cells is triggered by the interaction of a protein on the surface of the virus with a receptor angiotensin-converting enzyme 2 (ACE2) on the infected cells [2]. Preventing interaction between the viral protein on its surface and the cell receptor, using a soluble version of the viral receptor, angiotensinconverting enzyme 2 fused to an immunoglobulin Fc domain, is a proposed plan to prevent coronavirus infection [3]. This modified ACE2 will selectively interact with the viral protein and not with the cell, protecting physiological function of ACE2 [3]. Several viral enzymes are possible targets to design drugs for stopping viral infections. Once the virus penetrates into the host cell, it interferes with the genetic program. Possible target is the viral RNA-dependent RNA polymerases to avoid viral duplication. Remdesivir, a nucleotide analog, can inhibit the viral RNA-dependent RNA polymerase and had broad spectrum of antiviral activities against several RNA viruses including SARS-CoV and MERSCoV [4], stimulating hope that Remdesivir treatment could be also effective to treat
冠状病毒和酶:过去告诉我们什么?
新奇总是令人害怕,引发过度反应。另一方面,包括冠状病毒(COVID-19)在内的病毒感染策略自古以来就有,可以概括为:1)进入宿主细胞,2)干扰宿主遗传程序复制病毒实体;3)感染周围细胞。这些是病毒的优势,但也是它们的弱点,因为它确定了预防感染的可能目标。在病毒感染的每一步,都观察到病毒酶促反应,这可能与另一个密切相关的病毒家族中发生的反应相似。COVID-19与2018年在中国东部舟山采集的两种蝙蝠源性严重急性呼吸综合征(SARS)样冠状病毒(蝙蝠- slcovzc45和蝙蝠- sl - covzxc21)、SARS- cov(约79%)和MERS-CoV(约50%)[1]的相关性为88%。COVID-19与SARS-CoV类似,通过病毒表面的一种蛋白质与受感染细胞[2]上的受体血管紧张素转换酶2 (ACE2)相互作用触发进入受感染细胞。防止病毒蛋白表面与细胞受体之间的相互作用,使用病毒受体的可溶性版本,血管紧张素转换酶2融合到免疫球蛋白Fc结构域,是预防冠状病毒感染[3]的拟议计划。这种修饰的ACE2将选择性地与病毒蛋白相互作用,而不是与细胞相互作用,保护ACE2[3]的生理功能。几种病毒酶是设计阻止病毒感染药物的可能目标。一旦病毒进入宿主细胞,它就会干扰遗传程序。可能的目标是病毒依赖RNA的RNA聚合酶,以避免病毒复制。Remdesivir是一种核苷酸类似物,可以抑制病毒RNA依赖性RNA聚合酶,并对包括SARS-CoV和mers - scov[4]在内的几种RNA病毒具有广谱抗病毒活性,这激发了Remdesivir治疗也可能有效治疗的希望
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