The coronavirus disease 2019 (COVID-19) pandemic is driven by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, which has led to an enormous burden on patient morbidity and mortality. The renin–angiotensin–aldosterone system (RAAS) plays a significant role in various pulmonary diseases. Since SARS-CoV-2 utilizes the angiotensin-converting enzyme (ACE)2 receptor to exert its virulence and pathogenicity, the RAAS is of particular importance in COVID 19. Our preliminary study investigates retrospectively the influence of selected ACE-polymorphisms (I/D location at intron 16 in the B-coding sequence (rs4646994) and A-240T (rs 4291) at the A-promoter) as well as ACE1 and ACE2 serum levels on disease severity and the inflammatory response in inpatients and outpatients with COVID-19. Our study included 96 outpatients and 88 inpatients (65.9% male, mean age 60 years) with COVID-19 from April to December 2020 in four locations in Germany. Of the hospitalized patients, 88.6% participants were moderately ill (n = 78, 64% male, median age 60 years), and 11.4% participants were severely ill or deceased (n = 10, 90% male, median age 71 years). We found no polymorphism-related difference in disease, in age distribution, time to hospitalization and time of hospitalization for the inpatient group. ACE1 serum levels were significantly increased in the DD compared to the II polymorphism and in the TT compared to the AA polymorphism. There was no significant difference in ACE 1 serum levels l between moderately ill and severely ill patients. However, participants requiring oxygen supplementation had significantly elevated ACE1 levels compared to participants not requiring oxygen, with no difference in ACE2 levels whereas females had significantly higher ACE2 levels. Although there were no differences in the distribution of ACE polymorphisms in disease severity, we found increased proinflammatory regulation of the RAAS in patients with oxygen demand and increased serum ACE2 levels in women, indicating a possible enhanced anti-inflammatory immune response. Clinical trial registration: PreBiSeCov: German Clinical Trials Register, DRKS-ID: DRKS00021591, Registered on 27th April 2020.

中文翻译：

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ACE I 基因插入/缺失、A-240T 多态性和肾素-血管紧张素-醛固酮系统对 COVID-19 疾病的影响

2019 年冠状病毒病 (COVID-19) 大流行是由严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 感染驱动的，这给患者发病率和死亡率带来了巨大负担。肾素-血管紧张素-醛固酮系统（RAAS）在各种肺部疾病中发挥着重要作用。由于 SARS-CoV-2 利用血管紧张素转换酶 (ACE)2 受体发挥其毒力和致病性，因此 RAAS 在 COVID 19 中尤为重要。我们的初步研究回顾性地调查了所选 ACE 多态性 (I/D) 的影响B 编码序列中内含子 16 的位置（rs4646994）和 A 启动子处的 A-240T（rs 4291）以及 ACE1 和 ACE2 血清水平对 COVID-19 住院患者和门诊患者疾病严重程度和炎症反应的影响。我们的研究纳入了 2020 年 4 月至 12 月德国四个地点的 96 名门诊患者和 88 名住院患者（65.9% 为男性，平均年龄 60 岁）的 COVID-19 患者。在住院患者中，88.6% 的参与者患有中度疾病（n = 78，64% 男性，中位年龄 60 岁），11.4% 的参与者患有重病或死亡（n = 10，90% 男性，中位年龄 71 岁）。我们发现住院组的疾病、年龄分布、住院时间和住院时间没有与多态性相关的差异。与 II 多态性相比，DD 中的 ACE1 血清水平显着升高，与 AA 多态性相比，TT 中的 ACE1 血清水平显着升高。中度和重度患者血清ACE 1水平无显着差异。然而，与不需要吸氧的参与者相比，需要补充氧气的参与者的 ACE1 水平显着升高，而 ACE2 水平没有差异，而女性的 ACE2 水平显着较高。尽管 ACE 多态性在疾病严重程度方面的分布没有差异，但我们发现有氧需求的患者中 RAAS 的促炎调节增强，并且女性血清 ACE2 水平升高，表明抗炎免疫反应可能增强。临床试验注册：PreBiSeCov：德国临床试验注册中心，DRKS-ID：DRKS00021591，于2020年4月27日注册。