Abstract
Type I and III interferons (IFNs) and the nucleotide-binding
domain (NBD) leucine-rich repeat (LRR)-containing receptor
(NLR) family pyrin domain containing 3 (NLRP3) inflammasome
play pivotal roles in the pathogenesis of SARS-CoV-2.
While optimal IFN and inflammasome responses are essential
for limiting SARS-CoV-2 infection, aberrant activation of
these innate immune responses is associated with COVID-19
pathogenesis. In this review, we focus our discussion on recent
findings on SARS-CoV-2-induced type I and III IFNs
and NLRP3 inflammasome responses and the viral proteins
regulating these mechanisms.
Citations
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