Severe COVID-19: what have we learned with the immunopathogenesis?
Adv Rheumatol
; 60(1): 50, 2020 09 22.
Article
in English
| MEDLINE | ID: covidwho-781570
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.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Pneumonia, Viral
/
Respiratory Distress Syndrome
/
Coronavirus Infections
/
Betacoronavirus
/
Cytokine Release Syndrome
Type of study:
Experimental Studies
/
Observational study
/
Prognostic study
/
Randomized controlled trials
/
Reviews
Topics:
Long Covid
Limits:
Animals
/
Humans
Language:
English
Journal:
Adv Rheumatol
Year:
2020
Document Type:
Article
Affiliation country:
S42358-020-00151-7
Similar
MEDLINE
...
LILACS
LIS