Advances in Human Biology

REVIEW ARTICLE
Year
: 2022  |  Volume : 12  |  Issue : 2  |  Page : 114--119

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

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.


How to cite this article:
Zebardast A, Latifi T, Yavarian J. The role of severe acute respiratory syndrome coronavirus 2 viroporins in inflammation.Adv Hum Biol 2022;12:114-119


How to cite this URL:
Zebardast A, Latifi T, Yavarian J. The role of severe acute respiratory syndrome coronavirus 2 viroporins in inflammation. Adv Hum Biol [serial online] 2022 [cited 2022 Aug 11 ];12:114-119
Available from: https://www.aihbonline.com/article.asp?issn=2321-8568;year=2022;volume=12;issue=2;spage=114;epage=119;aulast=Zebardast;type=0