Perspective of molecular immune response of SARS-COV-2 infection

M. Rohmah, Arif Rahman Nurdianto
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引用次数: 7

Abstract

COVID-19 is a type of Pneumonia caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). When COVID-19 arise in Wuhan China and rapidly spread throughout to the World, we need to learn how pathogenesis and immune responses occur in the bodies in more detail. COVID-19 is the third Severe Respiratory Disease outbreak caused by the Coronavirus in the past two decades after Severe Acute Respiratory Syndrome (SARS) in the 2002 and Middle East Respiratory Syndrome (MERS) in 2012. The Articles from PUBMED and Research Gate were searched for studies on the immune response of COVID-19 infection by SARS-CoV-2. SARS-CoV-2 increases the number of neutrophils, suppresses IFN, increases the activity of Th1/Th17, B cells, CD8+ and CD4+, and causes cytokine storms especially pro-inflammatory cytokines which can increase respiration disorders and multi-organ damage. This review tries to explain about pathogenesis and immune responses of COVID-19 to provide a reference in designing the appropriate immune intervention for treatment and therapeutic such as drug or vaccine based on the recent research progress SARS-CoV-2 and previous studies about SARS CoV and MERS CoV.
严重急性呼吸系统综合征冠状病毒2型感染的分子免疫反应研究进展
COVID-19是一种由严重急性呼吸综合征冠状病毒2 (SARS-CoV-2)引起的肺炎。当COVID-19在中国武汉出现并迅速传播到世界各地时,我们需要更详细地了解体内的发病机制和免疫反应。COVID-19是继2002年的严重急性呼吸系统综合征(SARS)和2012年的中东呼吸综合征(MERS)之后,过去20年来由冠状病毒引起的第三次严重呼吸系统疾病暴发。检索PUBMED和Research Gate的文章,寻找SARS-CoV-2感染COVID-19的免疫应答研究。SARS-CoV-2增加中性粒细胞的数量,抑制IFN,增加Th1/Th17、B细胞、CD8+和CD4+的活性,并引起细胞因子风暴,特别是促炎细胞因子,可增加呼吸障碍和多器官损伤。本文结合SARS-CoV-2的最新研究进展以及SARS和MERS冠状病毒的相关研究,对COVID-19的发病机制和免疫应答进行阐述,为设计合适的药物或疫苗等免疫干预措施提供参考。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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