COVID-19 Molecular Pathophysiology: Acetylation of Repurposing Drugs.
Jong Hoon LeeBadar A KanwarAsif KhattakJenny BalentineNgoc Huy NguyenRichard Eric KastChul Joong LeeJean BourbeauEric L AltschulerConsolato Maria SergiTuan Ngoc Minh NguyenSangsuk OhMun-Gi SohnMichael D ColemanPublished in: International journal of molecular sciences (2022)
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.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- nuclear factor
- signaling pathway
- dendritic cells
- immune response
- toll like receptor
- pi k akt
- coronavirus disease
- low dose
- lps induced
- cardiovascular events
- histone deacetylase
- epithelial mesenchymal transition
- single molecule
- antiplatelet therapy
- induced apoptosis
- squamous cell carcinoma
- type diabetes
- inflammatory response
- cell proliferation
- gene expression
- genome wide
- acute coronary syndrome
- coronary artery disease
- pseudomonas aeruginosa
- staphylococcus aureus
- protein protein
- biofilm formation
- candida albicans