Coronavirus disease 19 (COVID-19) is a pandemic condition caused by the new coronavirus SARS-CoV-2. The typical symptoms are fever, cough, shortness of breath, evolving to a clinical picture of pneumonia and, ultimately, death. Nausea and diarrhea are equally frequent, suggesting viral infection or transmission via the gastrointestinal-enteric system. SARS-CoV-2 infects human cells by using angiotensin converting enzyme 2 (ACE2) as a receptor, which is cleaved by transmembrane proteases during host cells infection, thus reducing its activities. ACE2 is a relevant player in the renin-angiotensin system (RAS), counterbalancing the deleterious effects of angiotensin II. Furthermore, intestinal ACE2 functions as a chaperone for the aminoacid transporter B⁰AT1. It has been suggested that B⁰AT1/ACE2 complex in the intestinal epithelium regulates gut microbiota (GM) composition and function, with important repercussions on local and systemic immune responses against pathogenic agents, namely virus. Notably, productive infection of SARS-CoV-2 in ACE2⁺ mature human enterocytes and patients’ GM dysbiosis was recently demonstrated. This review outlines the evidence linking abnormal ACE2 functions with the poor outcomes (higher disease severity and mortality rate) in COVID-19 patients with pre-existing age-related comorbidities and addresses a possible role for GM dysbiosis. The article culminates with the therapeutics opportunities based on these pathways.

冠状病毒病 19 (COVID-19) 是由新型冠状病毒 SARS-CoV-2 引起的大流行病。典型的症状是发烧、咳嗽、呼吸急促，然后演变为肺炎的临床症状，最终导致死亡。恶心和腹泻同样频繁，表明病毒感染或通过胃肠道系统传播。SARS-CoV-2通过血管紧张素转换酶2（ACE2）作为受体感染人体细胞，在宿主细胞感染过程中被跨膜蛋白酶裂解，从而降低其活性。ACE2 是肾素-血管紧张素系统 (RAS) 的相关参与者，可抵消血管紧张素 II 的有害作用。此外，肠道 ACE2 还充当氨基酸转运体 B ⁰ AT1 的伴侣。有人建议 B ⁰肠上皮细胞中的 AT1/ACE2 复合物调节肠道微生物群 (GM) 的组成和功能，对针对病原体（即病毒）的局部和全身免疫反应产生重要影响。^{值得注意的是，最近证明了 ACE2 +}成熟人肠细胞中 SARS-CoV-2 的生产性感染和患者的 GM 生态失调。这篇综述概述了将异常 ACE2 功能与先前存在与年龄相关的合并症的 COVID-19 患者的不良结果（更高的疾病严重程度和死亡率）联系起来的证据，并解决了 GM 生态失调的可能作用。文章以基于这些途径的治疗机会作为结尾。