Severe COVID-19: what have we learned with the immunopathogenesis?
Adv Rheumatol
; 60: 50, 2020. graf
Article
en En
| LILACS
| ID: biblio-1130788
Biblioteca responsable:
BR1.1
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)
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
LILACS
Asunto principal:
Neumonía Viral
/
Infecciones por Coronavirus
/
Betacoronavirus
Tipo de estudio:
Clinical_trials
/
Etiology_studies
Límite:
Humans
Idioma:
En
Revista:
Adv Rheumatol
Asunto de la revista:
Artrite
/
Reumatologia
Año:
2020
Tipo del documento:
Article
País de afiliación:
Brasil
Pais de publicación:
Brasil