| Autor: |
Bordallo B; Departament of Internal Medicine / Emergence, Hospital Universitário Antônio Pedro / Univesidade Federal Fluminense, Niterói, RJ, Brazil. brunobaf@hotmail.com., Bellas M; Departament of Internal Medicine / Emergence, Hospital Universitário Antônio Pedro / Universidade Federal Fluminense, Niterói, RJ, Brazil., Cortez AF; Hospital Universitário Gaffré e Guinle / Universidade Federal do Estado do Rio de Janeiro, Internal Medicine Departament, Rio de Janeiro, RJ, Brazil., Vieira M; Departament of Internal Medicine, Hospital Universitário Clementino Fraga Filho, Rio de Janeiro, RJ, Brazil., Pinheiro M; Departament of Rheumatology, Universidade Federal de São Paulo, Sao Paulo, SP, Brazil. |
| Abstrakt: |
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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