| REVIEW ARTICLE |
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| Year : 2022 | Volume
: 12
| Issue : 2 | Page : 114-119 |
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The role of severe acute respiratory syndrome coronavirus 2 viroporins in inflammation
Arghavan Zebardast, Tayebeh Latifi, Jila Yavarian
Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
Correspondence Address:
Jila Yavarian
Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran
Iran
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/aihb.aihb_108_21
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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 β (IL1 β) and pro-IL18 by the caspase enzyme and convert them to the mature form (IL-1 β, 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.
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