Severe COVID-19: what have we learned with the immunopathogenesis?

Advances in Rheumatology

article

Bordallo, Bruno¹  Bellas, Mozart²  Cortez, Arthur Fernandes³  Vieira, Matheus⁴  Pinheiro, Marcelo⁵ 

[1] Departament of Internal Medicine / Emergence, Hospital Universitário Antônio Pedro / Univesidade Federal Fluminense;Departament of Internal Medicine / Emergence, Hospital Universitário Antônio Pedro / Universidade Federal Fluminense;Hospital Universitário Gaffré e Guinle / Universidade Federal do Estado do Rio de Janeiro, Internal Medicine Departament;Departament of Internal Medicine, Hospital Universitário Clementino Fraga Filho;Universidade Federal de São Paulo

关键词: COVID-19;    SARS-CoV-2;    Immunology;    Inflammation;    Cytokine storm;    Cytokine;    Macrophage activation syndrome;    Thrombosis;   

DOI  :  10.1186/s42358-020-00151-7

学科分类：地球科学(综合)

来源: Springer

【 摘 要 】

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.

【 授权许可】

CC BY