Severe COVID-19: what have we learned with the immunopathogenesis?
Severe COVID-19: what have we learned with the immunopathogenesis?
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DOI：
10.1186/s42358-020-00151-7
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发表时间：
2020-09-22
期刊：
影响因子：
--
通讯作者：
Pinheiro M
中科院分区：
文献类型：
--
作者：
Bordallo B;Bellas M;Cortez AF;Vieira M;Pinheiro M
由严重急性呼吸道综合征冠状病毒2型（SARS-CoV-2）引起的COVID-19疫情已成为全球主要关注的问题。在这篇综述中，我们提出了一个与严重的COVID-19相关的免疫发病机制的理论模型，基于SARS-CoV-2和其他流行性病原性冠状病毒，如SARS和MERS的现有文献。一些研究表明，SARS-CoV-2诱导的免疫失调和炎症反应比病毒本身更严重。COVID-19引起的免疫失调的特征是干扰素反应延迟和受损、淋巴细胞耗竭和细胞因子风暴，最终导致弥漫性肺组织损伤和后血栓形成现象。鉴于缺乏随机临床试验提供的临床证据，对SARS-CoV-2疾病发病机制和免疫应答的认识是制定基于合理性的临床治疗策略的基石。在这篇叙述性综述中，作者旨在描述重症COVID-19的免疫发病机制。
The COVID-19 outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global major concern. In this review, we addressed a theoretical model on immunopathogenesis associated with severe COVID-19, based on the current literature of SARS-CoV-2 and other epidemic pathogenic coronaviruses, such as SARS and MERS. Several studies have suggested that immune dysregulation and hyperinflammatory response induced by SARS-CoV-2 are more involved in disease severity than the virus itself. Immune dysregulation due to COVID-19 is characterized by delayed and impaired interferon response, lymphocyte exhaustion and cytokine storm that ultimately lead to diffuse lung tissue damage and posterior thrombotic phenomena. Considering there is a lack of clinical evidence provided by randomized clinical trials, the knowledge about SARS-CoV-2 disease pathogenesis and immune response is a cornerstone to develop rationale-based clinical therapeutic strategies. In this narrative review, the authors aimed to describe the immunopathogenesis of severe forms of COVID-19.
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