Severe COVID-19: what have we learned with the immunopathogenesis?
Adv Rheumatol
;
60: 50, 2020. graf
Article
in English
| LILACS
| ID: biblio-1130788
ABSTRACT
Abstract 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.(AU)
Full text:
Available
Index:
LILACS (Americas)
Main subject:
Pneumonia, Viral
/
Coronavirus Infections
/
Betacoronavirus
Type of study:
Controlled clinical trial
/
Etiology study
Limits:
Humans
Language:
English
Journal:
Adv Rheumatol
Journal subject:
Artrite
/
Reumatologia
Year:
2020
Type:
Article
Affiliation country:
Brazil
Institution/Affiliation country:
Hospital Universitário Clementino Fraga Filho/BR
/
Universidade Federal Fluminense/BR
/
Universidade Federal de São Paulo/BR
/
Universidade Federal do Estado do Rio de Janeiro/BR
/
Univesidade Federal Fluminense/BR
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