Possible protective role of 17β-estradiol against COVID-19.

Journal of allergy and infectious diseases Pub Date : 2020-01-01 Epub Date: 2020-08-19 DOI:10.46439/allergy.1.010
Nabab Khan
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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.

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17β-雌二醇对COVID-19可能的保护作用。
严重急性呼吸综合征-冠状病毒2 (SARS-CoV-2)是导致2019冠状病毒病(COVID-19)的病毒;世界卫生组织(世卫组织)宣布的全球性流行病。SARS-CoV-2似乎是通过首先与膜相关血管紧张素转换酶2 (ACE2)和跨膜蛋白酶丝氨酸2 (TMPRSS2)结合并启动其病毒刺突蛋白来感染细胞的。通过ACE2和TMPRSS2的协同作用,SARS-CoV-2刺突蛋白与质膜融合,最终病毒进入细胞。ACE2是肾素-血管紧张素-醛固酮系统(RAAS)的组成部分,SARS-CoV-2下调ACE2的蛋白表达水平。一旦感染,患者通常会出现急性呼吸窘迫综合征(ARDS)和许多其他严重并发症,导致高死亡率,特别是老年人(60岁以上)和已有疾病的人。现在的数据清楚地表明,在所有年龄组中,男性COVID-19死亡人数高于女性。本文将重点关注这些性别差异,并推测雌激素在这些差异中的作用,以及17β-雌二醇对COVID-19可能的治疗和保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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