{"title":"Coronavirus and Enzymes: What the Past Told us?","authors":"Hortense Ferriz, R. Buchet","doi":"10.2174/0218749402005010001","DOIUrl":null,"url":null,"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","PeriodicalId":89033,"journal":{"name":"The open enzyme inhibition journal","volume":"5 1","pages":"1-1"},"PeriodicalIF":0.0000,"publicationDate":"2020-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The open enzyme inhibition journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/0218749402005010001","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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