Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiologic agent of coronavirus disease 19 (COVID-19), and is genetically related to the 2003 SARS and Middle East respiratory syndrome (MERS-CoV) coronaviruses. Recent studies have reported that similar to SARS-CoV, this strain expresses a spike protein (S) with a receptor binding domain (RBD) that binds to angiotensin-converting enzyme 2 (ACE2) – an enzyme expressed mostly in the endothelium, kidneys, heart, gastrointestinal tract and lungs – to facilitate viral entry and intracellular replication. Incidentally, the renin-angiotensin-aldosterone system (RAAS) is integral to physiologic control of both ACE and ACE2 expression, and is an essential system utilized by SARS-CoV-2, albeit with varying schools of thought on how it can affect viral entry. In this paper, we will review current knowledge on the RAAS and how it can be affected by non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroid use at the organ and cellular levels. We will then discuss the relevance of these interactions on organ-specific ACE2 expression, and provide scientific insights on how this mechanism can potentially affect SARS-CoV-2 infection in the early phases of disease. From the standpoint of other known viruses, we will then aim to discuss the potential uses or restrictions of these drugs in viral infection, and provide an update on relevant studies about COVID-19.

严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 是冠状病毒病 19 (COVID-19) 的病原体，与 2003 年 SARS 和中东呼吸综合征 (MERS-CoV) 冠状病毒在基因上相关。最近的研究报告称，与 SARS-CoV 类似，该病毒株表达具有受体结合域 (RBD) 的刺突蛋白 (S)，该受体结合域 (RBD) 与血管紧张素转换酶 2 (ACE2) 结合，血管紧张素转换酶 2 是一种主要在内皮、肾脏、心脏、胃肠道和肺——促进病毒进入和细胞内复制。顺便说一句，肾素-血管紧张素-醛固酮系统 (RAAS) 是 ACE 和 ACE2 表达的生理控制不可或缺的一部分，也是 SARS-CoV-2 使用的一个重要系统，尽管对于它如何影响病毒进入有不同的看法。在本文中，我们将回顾目前关于 RAAS 的知识，以及非甾体抗炎药 (NSAID) 和皮质类固醇在器官和细胞水平上的使用如何影响它。然后，我们将讨论这些相互作用与器官特异性 ACE2 表达的相关性，并就这种机制如何可能影响疾病早期阶段的 SARS-CoV-2 感染提供科学见解。然后，我们将从其他已知病毒的角度出发，讨论这些药物在病毒感染中的潜在用途或限制，并提供有关 COVID-19 的相关研究的最新信息。