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Coronavirus disease - COVID-19

KEGG ID: hsa05171

中文名称

2019 年冠状病毒病 - COVID-19

通路描述

2019 年冠状病毒病(COVID-19)是由严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)引起的一种高度传染性的呼吸道疾病。SARS-CoV-2 通过血管紧张素转换酶 2(ACE2)受体感染肺泡上皮细胞(主要是肺泡上皮 2 型细胞)。当 SARS-CoV-2 占据 ACE2 时,由于 ACE2 介导的降解减少,导致血清中游离血管紧张素 II(Ang II)水平增加,促进通过血管紧张素 II 型 1 受体(AT1R)激活 NF-κB 途径,随后产生白细胞介素 -6(IL-6)。SARS-CoV-2 还激活先天免疫系统;巨噬细胞刺激导致促炎细胞因子(包括 IL-6)的过度产生,引发“细胞风暴”,导致全身性炎症反应综合征和多器官功能障碍。补体激活、失调的中性粒细胞增多、内皮损伤和凝血异常似乎相互交织,以驱动 COVID-19 的严重特征。
英文描述
Coronavirus disease of 2019 (COVID-19) is a highly contagious respiratory infection that is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 infects alveolar epithelial cells [mainly alveolar epithelial type 2 (AEC2) cells] through the angiotensin-converting enzyme 2 (ACE2) receptor. Upon the occupancy of ACE2 by SARS-CoV-2, the increased serum level of free Angiotensin II (Ang II) due to a reduction of ACE2-mediated degradation promotes activation of the NF-kappa B pathway via Ang II type 1 receptor (AT1R), followed by interleukin-6 (IL-6) production. SARS-CoV-2 also activates the innate immune system; macrophage stimulation triggers the overproduction of pro-inflammatory cytokines, including IL-6, and the "cytokine storm", which results in systemic inflammatory response syndrome and multiple organ failure. The combined effects of complement activation, dysregulated neutrophilia, endothelial injury, and hypercoagulability appear to be intertwined to drive the severe features of COVID-19.

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