Lessons Learned from Coronavirus Disease 2019 Sex Disparities.
Lessons Learned from Coronavirus Disease 2019 Sex Disparities.
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从 2019 年冠状病毒病性别差异中吸取的教训。
DOI：
10.1089/jwh.2021.0110
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发表时间：
2021
期刊：
影响因子：
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通讯作者：
Volgman,AnnabelleSantos
中科院分区：
文献类型：
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作者：
Suboc,Tisha;Gomez,JoanneMichelleD;Volgman,Caroline;Volgman,AnnabelleSantos
本期《妇女健康杂志》揭示了纽约大流行早期最广泛的报告之一的重要发现。Tejpal等人的文章显示，在美国，与女性相比，男性在感染严重急性呼吸系统综合征（SARS）-Cov-2病毒（2019冠状病毒病[COVID-19]）时的死亡率更高-他们发现女性感染COVID-19的住院死亡风险降低了27%。[1]尽管这一发现对于COVID-19来说是新的，但对一种相关的传染病也有类似的观察。早在2003年，中国内地和香港的数据就显示，在调整年龄后，男性感染SARS的死亡率远高于女性，分别为21.0%和13.2%。2.男女之间SARS和COVID-19临床结果的性别差异的生物学根源可能是多因素的。性是通过许多机制表达的，这些机制可能在差异中发挥作用，包括性别特异性行为，遗传和激素因素以及不同的生物途径。肾素-血管紧张素-醛固酮系统（RAAS）是SARS-CoV-2疾病发病机制的核心，是一系列最终形成血管紧张素II（Ang II）的催化步骤。血管紧张素转换酶2（ACE 2）是RAAS的负调节因子，具有保护性调节作用。它通过Ang II的失活和转化为Ang 1-7来调节该过程，Ang 1- 7是一种随后激活Mas受体（MasR）的肽-一种导致抗炎、抗纤维化和血管舒张作用的级联反应。3，4对SARS-CoV-2的研究表明，它直接与ACE 2受体相互作用，病毒依赖ACE 2进入细胞。通过这个过程，SARS-CoV-2感染最终减少了保护性ACE 2的量，导致更高的病毒载量和疾病严重程度。也可能有可溶性形式的ACE 2与病毒结合，从而阻止其中一些与细胞ACE 2受体结合，降低疾病严重程度，改善预后。女性的优势可能是由于额外的X染色体，因为负责先天免疫和适应性免疫的多个基因以及ACE 2位于X染色体上。3，4与男性相比，女性的肺泡II型细胞表达ACE 2较少。此外，
This issue of the Journal of Women’s Health brings to light an important finding from one of the most extensive reports from the early period of the pandemic in New York. The article by Tejpal et al. shows that in the United States, men compared with women have a higher mortality rate when infected with the severe acute respiratory syndrome (SARS)-Cov-2 virus (coronavirus disease 2019 [COVID-19])—they found that women had a 27% lower risk of inhospital mortality with COVID-19. 1 Although this finding is new for COVID-19, similar observations have been made of a related infectious disease. As early as 2003, data from China and Hong Kong revealed that men’s mortality rate was much higher than that of women infected with SARS after adjusting for age, 21.0% versus 13.2%. 2 The biological origin of the sex disparity in clinical outcomes of both SARS and COVID-19 between men and women is likely multifactorial. Sex is expressed through many mechanisms that could play a role in the disparity, including gender-specific behaviors, genetic and hormonal factors, and distinct biological pathways. Renin–angiotensin–aldosterone system (RAAS), a series of catalytic steps culminating in the formation of angiotensin (Ang) II, is central in the pathogenesis of SARS-CoV-2 disease. Angiotensin-converting enzyme 2 (ACE2) is a negative regulator of RAAS with protective regulatory effects. It regulates the process through Ang II’s deactivation and conversion into Ang 1–7, a peptide that subsequently activates the Mas receptor (MasR)—a cascade leading to anti-inflammatory, antifibrotic, and vasodilatory effects. 3, 4 Studies of SARS-CoV-2 reveal that it directly interacts with ACE2 receptors and that the virus relies on ACE2 for cellular entry. Through this process, SARS-CoV-2 infection ultimately reduces the amount of protective ACE2, resulting in a higher viral load and disease severity. 4 There may also be soluble forms of ACE2 that may bind to the virus, thereby preventing some of it from binding to the cellular ACE2 receptors, reducing disease severity, and improving outcomes. 5The female advantage may be due to the extra X chromosome, as multiple genes responsible for innate and adaptive immunity, and ACE2, are located on the X chromosomes. 3, 4 Women have been shown to have less pulmonary alveolar type II cells expressing ACE2 compared with men. In addi-