Can endolysosomal deacidification and inhibition of autophagy prevent severe COVID-19?
Antiviral treatment
COVID-19
Immunomodulation
Macrolide
SARS-CoV-2
Journal
Life sciences
ISSN: 1879-0631
Titre abrégé: Life Sci
Pays: Netherlands
ID NLM: 0375521
Informations de publication
Date de publication:
01 Dec 2020
01 Dec 2020
Historique:
received:
25
08
2020
revised:
28
09
2020
accepted:
29
09
2020
pubmed:
10
10
2020
medline:
15
12
2020
entrez:
9
10
2020
Statut:
ppublish
Résumé
The possibility is examined that immunomodulatory pharmacotherapy may be clinically useful in managing the pandemic coronavirus disease 2019 (COVID-19), known to result from infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a positive-sense single-stranded RNA virus. The dominant route of cell entry of the coronavirus is via phagocytosis, with ensconcement in endosomes thereafter proceeding via the endosomal pathway, involving transfer from early (EEs) to late endosomes (LEs) and ultimately into lysosomes via endolysosomal fusion. EE to LE transportation is a rate-limiting step for coronaviruses. Hence inhibition or dysregulation of endosomal trafficking could potentially inhibit SARS-CoV-2 replication. Furthermore, the acidic luminal pH of the endolysosomal system is critical for the activity of numerous pH-sensitive hydrolytic enzymes. Golgi sub-compartments and Golgi-derived secretory vesicles also depend on being mildly acidic for optimal function and structure. Activation of endosomal toll-like receptors by viral RNA can upregulate inflammatory mediators and contribute to a systemic inflammatory cytokine storm, associated with a worsened clinical outcome in COVID-19. Such endosomal toll-like receptors could be inhibited by the use of pharmacological agents which increase endosomal pH, thereby reducing the activity of acid-dependent endosomal proteases required for their activity and/or assembly, leading to suppression of antigen-presenting cell activity, decreased autoantibody secretion, decreased nuclear factor-kappa B activity and decreased pro-inflammatory cytokine production. It is also noteworthy that SARS-CoV-2 inhibits autophagy, predisposing infected cells to apoptosis. It is therefore also suggested that further pharmacological inhibition of autophagy might encourage the apoptotic clearance of SARS-CoV-2-infected cells.
Identifiants
pubmed: 33035581
pii: S0024-3205(20)31294-7
doi: 10.1016/j.lfs.2020.118541
pmc: PMC7537668
pii:
doi:
Substances chimiques
Antiviral Agents
0
Hydroxychloroquine
4QWG6N8QKH
Azithromycin
83905-01-5
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
118541Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
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