The role of severe acute respiratory syndrome coronavirus 2 viroporins in inflammation
Advances in Human Biology
; 12(2):114-119, 2022.
Article
in English
| Web of Science | ID: covidwho-2155509
ABSTRACT
In December 2019, genomic screening of clinical samples from patients with viral pneumonia in Wuhan, China, revealed the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is the official name for the disease caused by this virus, according to the World Health Organization. SARS-CoV-2 can activate the NLRP3 inflammasome directly in apoptosis-associated speck-like protein (ASC)-dependent or independent manner through several proteins, including viroporins. Viroporins are viral proteins with ion channel functions that play crucial roles in different aspects of virus replication and pathogenesis. SARS-CoV-2 viroporins encoded by Open Reading Frame (ORF) 3a, ORF8 and the E gene activate the NLRP3 inflammasome and trigger the cleavages of pro-interleukin 1 beta (IL1 beta) and pro-IL18 by the caspase enzyme and convert them to the mature form (IL-1 beta, IL18). Most of the inflammation in severe COVID-19 patients is caused by the activation of inflammasomes. Studies revealed that SARS-CoV-2 viroporins could be the possible targets for therapeutic interventions.
Full text:
Available
Collection:
Databases of international organizations
Database:
Web of Science
Language:
English
Journal:
Advances in Human Biology
Year:
2022
Document Type:
Article
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