A novel hypothesis for COVID-19 pathogenesis: Retinol depletion and retinoid signaling disorder.
COVID-19
/ immunology
Central Nervous System
/ metabolism
DEAD Box Protein 58
/ metabolism
Humans
Immune Tolerance
Interferon Type I
/ metabolism
Receptors, Immunologic
/ metabolism
SARS-CoV-2
/ genetics
Signal Transduction
/ physiology
T-Lymphocytes, Regulatory
/ immunology
Viral Tropism
/ physiology
Vitamin A
/ blood
Autoimmunity
COVID-19
CYP450
FoxP3
Inflammation
NF-κB
RIG-I
RORγt
Retinoic acid
Retinoid signaling
Retinol
Th17
Treg
Type-I IFN
Vitamin A
Vitamin D
Journal
Cellular signalling
ISSN: 1873-3913
Titre abrégé: Cell Signal
Pays: England
ID NLM: 8904683
Informations de publication
Date de publication:
11 2021
11 2021
Historique:
received:
18
03
2021
revised:
18
08
2021
accepted:
19
08
2021
pubmed:
27
8
2021
medline:
14
10
2021
entrez:
26
8
2021
Statut:
ppublish
Résumé
The SARS-CoV-2 virus has caused a worldwide COVID-19 pandemic. In less than a year and a half, more than 200 million people have been infected and more than four million have died. Despite some improvement in the treatment strategies, no definitive treatment protocol has been developed. The pathogenesis of the disease has not been clearly elucidated yet. A clear understanding of its pathogenesis will help develop effective vaccines and drugs. The immunopathogenesis of COVID-19 is characteristic with acute respiratory distress syndrome and multiorgan involvement with impaired Type I interferon response and hyperinflammation. The destructive systemic effects of COVID-19 cannot be explained simply by the viral tropism through the ACE2 and TMPRSS2 receptors. In addition, the recently identified mutations cannot fully explain the defect in all cases of Type I interferon synthesis. We hypothesize that retinol depletion and resulting impaired retinoid signaling play a central role in the COVID-19 pathogenesis that is characteristic for dysregulated immune system, defect in Type I interferon synthesis, severe inflammatory process, and destructive systemic multiorgan involvement. Viral RNA recognition mechanism through RIG-I receptors can quickly consume a large amount of the body's retinoid reserve, which causes the retinol levels to fall below the normal serum levels. This causes retinoid insufficiency and impaired retinoid signaling, which leads to interruption in Type I interferon synthesis and an excessive inflammation. Therefore, reconstitution of the retinoid signaling may prove to be a valid strategy for management of COVID-19 as well for some other chronic, degenerative, inflammatory, and autoimmune diseases.
Identifiants
pubmed: 34438017
pii: S0898-6568(21)00210-2
doi: 10.1016/j.cellsig.2021.110121
pmc: PMC8380544
pii:
doi:
Substances chimiques
Interferon Type I
0
Receptors, Immunologic
0
Vitamin A
11103-57-4
RIGI protein, human
EC 3.6.1.-
DEAD Box Protein 58
EC 3.6.4.13
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
110121Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.
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