Zebardast Arghavan, Hasanzadeh Ali, Ebrahimian Shiadeh Seyedeh Arefeh, Tourani Mehdi, Yahyapour Yousef
Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Department of Microbiology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran.
Cell Biol Int. 2023 May;47(5):848-858. doi: 10.1002/cbin.11997. Epub 2023 Feb 5.
The SARS-coronavirus-2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19), has spread worldwide and caused a global health emergency. SARS-CoV-2 is a coronaviridae virus that infects target cells by interacting with the plasma membrane-expressed angiotensin-converting enzyme 2 (ACE2) via the S1 component of the S protein. Effective host immune response to SARS-CoV-2 infection, which includes both innate and adaptive immunity, is critical for virus management and elimination. The intensity and outcome of COVID-19 may be related to an overabundance of pro-inflammatory cytokines, which results in a "cytokine storm" and acute respiratory distress syndrome. After SARS-CoV-2 infection, the immune system's hyperactivity and production of autoantibodies may result in autoimmune diseases such as autoimmune hemolytic anemia, autoimmune thrombocytopenia, Guillain-Barré syndrome, vasculitis, multiple sclerosis, pro-thrombotic state, and diffuse coagulopathy, as well as certain autoinflammatory conditions such as Kawasaki disease in children. We have reviewed the association between COVID-19 and autoimmune disorders in this article.
导致2019冠状病毒病(COVID-19)的严重急性呼吸综合征冠状病毒2(SARS-CoV-2)已在全球传播,并引发了全球卫生紧急事件。SARS-CoV-2是一种冠状病毒科病毒,它通过S蛋白的S1成分与质膜表达的血管紧张素转换酶2(ACE2)相互作用来感染靶细胞。宿主对SARS-CoV-2感染的有效免疫反应,包括固有免疫和适应性免疫,对于病毒的控制和清除至关重要。COVID-19的严重程度和结果可能与促炎细胞因子的过量产生有关,这会导致“细胞因子风暴”和急性呼吸窘迫综合征。SARS-CoV-2感染后,免疫系统的过度活跃和自身抗体的产生可能导致自身免疫性疾病,如自身免疫性溶血性贫血、自身免疫性血小板减少症、吉兰-巴雷综合征、血管炎、多发性硬化症、血栓前状态和弥漫性凝血病,以及某些自身炎症性疾病,如儿童川崎病。我们在本文中综述了COVID-19与自身免疫性疾病之间的关联。