COVID-19 Molecular Pathophysiology: Acetylation of Repurposing Drugs.
Int J Mol Sci
; 23(21)2022 Oct 31.
Article
in English
| MEDLINE | ID: covidwho-2099576
ABSTRACT
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces immune-mediated type 1 interferon (IFN-1) production, the pathophysiology of which involves sterile alpha motif and histidine-aspartate domain-containing protein 1 (SAMHD1) tetramerization and the cytosolic DNA sensor cyclic-GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway. As a result, type I interferonopathies are exacerbated. Aspirin inhibits cGAS-mediated signaling through cGAS acetylation. Acetylation contributes to cGAS activity control and activates IFN-1 production and nuclear factor-κB (NF-κB) signaling via STING. Aspirin and dapsone inhibit the activation of both IFN-1 and NF-κB by targeting cGAS. We define these as anticatalytic mechanisms. It is necessary to alleviate the pathologic course and take the lag time of the odds of achieving viral clearance by day 7 to coordinate innate or adaptive immune cell reactions.
Keywords
ACE2 (angiotensin-converting enzyme 2); SAMHD1 (sterile alpha motif and histidine-aspartate domain-containing protein 1); SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2); TLR4 (Toll-like receptor 4); aspirin; cGASSTING (cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) synthase (cGAS)stimulator of interferon genes (STING)); dapsone; dexamethasone; immunologic engram; inflammasome; spike protein
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Interferon Type I
/
COVID-19 Drug Treatment
Type of study:
Prognostic study
Limits:
Humans
Language:
English
Year:
2022
Document Type:
Article
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