{"title":"Possible protective role of 17β-estradiol against COVID-19.","authors":"Nabab Khan","doi":"10.46439/allergy.1.010","DOIUrl":null,"url":null,"abstract":"<p><p>Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) is the virus that causes coronavirus disease 2019 (COVID-19); a worldwide pandemic as declared by the World Health Organization (WHO). SARS-CoV-2 appears to infect cells by first binding and priming its viral-spike proteins with membrane-associated angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). Through the coordinated actions of ACE2 and TMPRSS2, SARS-CoV-2 spike proteins fuse with plasma membranes and ultimately the virus enters cells. ACE2 is integral to the renin-angiotensin-aldosterone system (RAAS), and SARS-CoV-2 down-regulates protein expression levels of ACE2. Once infected, patients typically develop acute respiratory distress syndrome (ARDS) and a number of other severe complications that result in a high rate of fatality, especially in older (>60 years) adults and in people with pre-existing medical conditions. Data now indicate clearly that among people of all age groups, COVID-19 fatalities are higher in men than women. Here, attention is focused on these sex differences and posit a role of estrogen in these differences as well as possible therapeutic and protective actions of 17β-estradiol against COVID-19.</p>","PeriodicalId":73592,"journal":{"name":"Journal of allergy and infectious diseases","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7665224/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of allergy and infectious diseases","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.46439/allergy.1.010","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/8/19 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) is the virus that causes coronavirus disease 2019 (COVID-19); a worldwide pandemic as declared by the World Health Organization (WHO). SARS-CoV-2 appears to infect cells by first binding and priming its viral-spike proteins with membrane-associated angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). Through the coordinated actions of ACE2 and TMPRSS2, SARS-CoV-2 spike proteins fuse with plasma membranes and ultimately the virus enters cells. ACE2 is integral to the renin-angiotensin-aldosterone system (RAAS), and SARS-CoV-2 down-regulates protein expression levels of ACE2. Once infected, patients typically develop acute respiratory distress syndrome (ARDS) and a number of other severe complications that result in a high rate of fatality, especially in older (>60 years) adults and in people with pre-existing medical conditions. Data now indicate clearly that among people of all age groups, COVID-19 fatalities are higher in men than women. Here, attention is focused on these sex differences and posit a role of estrogen in these differences as well as possible therapeutic and protective actions of 17β-estradiol against COVID-19.