Severe COVID-19: what have we learned with the immunopathogenesis?
Adv Rheumatol
; 60:50-50, 2020.
Article
in English
| LILACS (Americas) | ID: grc-742198
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.
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Collection:
Databases of international organizations
Database:
LILACS (Americas)
Type of study:
Experimental Studies
/
Prognostic study
/
Randomized controlled trials
/
Reviews
Language:
English
Journal:
Adv Rheumatol
Year:
2020
Document Type:
Article
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