Coronaviruses (CoVs) contribute significantly to the burden of respiratory diseases, frequently as upper respiratory tract infections. Recent emergence of novel coronaviruses in the last few decades has highlighted the potential transmission, disease, and mortality related to these viruses. In this literature review, we shall explore the disease-causing mechanism of the virus through human monocytes and macrophages. Common strains will be discussed; however, this review will center around coronaviruses responsible for epidemics, namely severe acute respiratory syndrome coronavirus (SARS-CoV)-1 and -2 and the Middle East Respiratory Syndrome Coronavirus (MERS-CoV). Macrophages are key players in the immune system and have been found to play a role in the pathogenesis of lethal coronaviruses. In physiology, they are white blood cells that engulf and digest cellular debris, foreign substances, and microbes. They play a critical role in innate immunity and help initiate adaptive immunity. Human coronaviruses utilize various mechanisms to undermine the innate immune response through its interaction with macrophages and monocytes. It is capable of entering immune cells through DPP4 (dipeptidyl-peptidase 4) receptors and antibody-dependent enhancement, delaying initial interferon response which supports robust viral replication. Pathogenesis includes triggering the production of overwhelming pro-inflammatory cytokines that attract other immune cells to the site of infection, which propagate prolonged pro-inflammatory response. The virus has also been found to suppress the release of anti-inflammatory mediators such as IL-10, leading to an aberrant inflammatory response. Elevated serum cytokines are also believed to contribute to pathological features seen in severe disease such as coagulopathy, acute lung injury, and multiorgan failure.

中文翻译：

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冠状病毒通过人单核细胞和组织巨噬细胞的发病机制

冠状病毒 (CoV) 显着增加了呼吸道疾病的负担，通常是上呼吸道感染。近几十年来，新型冠状病毒的出现凸显了与这些病毒相关的潜在传播、疾病和死亡率。在这篇文献综述中，我们将通过人类单核细胞和巨噬细胞探索病毒的致病机制。将讨论常见的菌株；然而，本次审查将围绕导致流行病的冠状病毒展开，即严重急性呼吸综合征冠状病毒 (SARS-CoV)-1 和 -2 以及中东呼吸综合征冠状病毒 (MERS-CoV)。巨噬细胞是免疫系统的关键参与者，已被发现在致命冠状病毒的发病机制中发挥作用。在生理学上，它们是吞噬和消化细胞碎片、外来物质和微生物的白细胞。它们在先天免疫中起着关键作用，并有助于启动适应性免疫。人类冠状病毒利用各种机制通过其与巨噬细胞和单核细胞的相互作用来破坏先天免疫反应。它能够通过 DPP4（二肽基肽酶 4）受体和抗体依赖性增强进入免疫细胞，延迟支持强大病毒复制的初始干扰素反应。发病机制包括触发大量促炎细胞因子的产生，这些细胞因子将其他免疫细胞吸引到感染部位，从而传播延长的促炎反应。还发现该病毒可抑制抗炎介质如 IL-10 的释放，导致异常的炎症反应。升高的血清细胞因子也被认为是导致严重疾病（如凝血病、急性肺损伤和多器官衰竭）的病理特征的原因。