Department of Biochemistry, School of Bioengineering and Biosciences, Lovely Professional University, Phagwara, Punjab, India.
Department of Chemistry, School of Chemical Engineering and Physical Science, Lovely Professional University, Phagwara, Punjab, India.
Clin Immunol. 2021 Oct;231:108842. doi: 10.1016/j.clim.2021.108842. Epub 2021 Aug 27.
Severe acute respiratory syndrome coronavirus-2 causes coronavirus disease 2019, a pandemic which was originated from Wuhan city of China. The pandemic has affected millions of people worldwide. The pathogenesis of SARS-CoV-2 is characterized by a cytokine storm in the blood (cytokinemia) and tissues, especially the lungs. One of the major repercussions of this inflammatory process is the endothelial injury-causing intestinal bleeding, coagulopathy, and thromboembolism which result in various sudden and unexpected post-COVID complications including kidney failure, myocardial infarction, or multiorgan failure. In this review, we have summarized the immune responses, biochemical changes, and inflammatory responses in the human body after infection with the SARS-CoV-2 virus. The increased amount of inflammatory cytokines, chemokines, and involvement of complement proteins in inflammatory reaction increase the risk of occurrence of disease.
严重急性呼吸综合征冠状病毒 2 引起 2019 年冠状病毒病，这是一种起源于中国武汉市的大流行疾病。该大流行疾病已影响了全球数百万人。SARS-CoV-2 的发病机制以血液（细胞因子血症）和组织中的细胞因子风暴为特征，特别是肺部。该炎症过程的主要后果之一是内皮损伤导致肠道出血、凝血功能障碍和血栓栓塞，从而导致各种突发和意外的新冠病毒感染后并发症，包括肾衰竭、心肌梗死或多器官衰竭。在这篇综述中，我们总结了人体感染 SARS-CoV-2 病毒后的免疫反应、生化变化和炎症反应。炎症反应中炎症细胞因子、趋化因子的增加量和补体蛋白的参与增加了疾病发生的风险。
