Severe COVID-19: what have we learned with the immunopathogenesis?
Adv Rheumatol
;
60: 50, 2020. graf
Article
Dans Anglais
| 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)
Texte intégral:
Disponible
Indice:
LILAS (Amériques)
Sujet Principal:
Pneumopathie virale
/
Infections à coronavirus
/
Betacoronavirus
Type d'étude:
Essai clinique contrôlé
/
Etude d'étiologie
Limites du sujet:
Humains
langue:
Anglais
Texte intégral:
Adv Rheumatol
Thème du journal:
Artrite
/
Reumatologia
Année:
2020
Type:
Article
Pays d'affiliation:
Brésil
Institution/Pays d'affiliation:
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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