Aggravating mechanisms from COVID-19.
CGAS–STING
COVID-19
Inflammasome
NLRP3
SAMHD1
SARS-CoV-2
Journal
Virology journal
ISSN: 1743-422X
Titre abrégé: Virol J
Pays: England
ID NLM: 101231645
Informations de publication
Date de publication:
27 Sep 2024
27 Sep 2024
Historique:
received:
08
08
2024
accepted:
16
09
2024
medline:
28
9
2024
pubmed:
28
9
2024
entrez:
28
9
2024
Statut:
epublish
Résumé
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces immune-mediated diseases. The pathophysiology of COVID-19 uses the following three mechanisms: (1) inflammasome activation mechanism; (2) cGAS-STING signaling mechanism; and (3) SAMHD1 tetramerization mechanism, which leads to IFN-I production. Interactions between the host and virus govern induction, resulting in multiorgan impacts. The NLRP3 with cGAS-STING constitutes the primary immune response. The expression of SARS-CoV-2 ORF3a, NSP6, NSP7, and NSP8 blocks innate immune activation and facilitates virus replication by targeting the RIG-I/MDA5, TRIF, and cGAS-STING signaling. SAMHD1 has a target motif for CDK1 to protect virion assembly, threonine 592 to modulate a catalytically active tetramer, and antiviral IFN responses to block retroviral infection. Plastic and allosteric nucleic acid binding of SAMHD1 modulates the antiretroviral activity of SAMHD1. Therefore, inflammasome activation, cGAS-STING signaling, and SAMHD1 tetramerization explain acute kidney injury, hepatic, cardiac, neurological, and gastrointestinal injury of COVID-19. It might be necessary to effectively block the pathological courses of diverse diseases.
Identifiants
pubmed: 39334442
doi: 10.1186/s12985-024-02506-8
pii: 10.1186/s12985-024-02506-8
doi:
Substances chimiques
Inflammasomes
0
cGAS protein, human
EC 2.7.7.-
SAM Domain and HD Domain-Containing Protein 1
EC 3.1.5.-
Nucleotidyltransferases
EC 2.7.7.-
STING1 protein, human
0
Membrane Proteins
0
SAMHD1 protein, human
EC 3.1.5.-
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
228Informations de copyright
© 2024. The Author(s).
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