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严重急性呼吸综合征冠状病毒2(severe acute respiratory syndrome coronavirus 2, SARS-CoV-2)属于β冠状病毒，其通过表面刺突蛋白(spike protein, S蛋白)以血管紧张素转换酶2(angiotensin-converting enzyme 2, ACE2)作为受体介导膜融合入侵宿主细胞。感染过程中造成的功能性ACE2水平下降通过影响肾素血管紧张素系统(renin-angiotensin system, RAS)的平衡造成肺部损伤。感染SARS-CoV-2的部分重症感染患者中，机体先天和适应性免疫机制的失衡而形成的细胞因子风暴，可导致急性呼吸窘迫综合征(acute respiratory distress syndrome, ARDS)及全身多器官功能脏器衰竭。适应性免疫的失衡所致淋巴细胞总数的降低，并与不良预后相关。“,”The novel coronavirus severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) is a beta coronavirus that mediates the incorporation of angiotensin-converting enzyme 2(ACE2 )as a receptor into invading host cells via the surface S protein. In patients with severe SARS-CoV-2 infection, an imbalance between the innate and adaptive immune mechanisms leads to the formation of a cytokine storm, resulting in acute respiratory distress syndrome and systemic multiorgan failure. The imbalance of the immune system in adaptive immunity leads to a decrease in the total number of lymphocytes and is associated with poor prognosis.