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. 2021 Jun 1;22(11):5992. doi: 10.3390/ijms22115992

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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The impact of coronavirus infection on innate immune responses. Phosphorylation of eIF2α is triggered by the PKR/PERK pathway and leads to reduced IκB synthesis. Activated IRE1 binds to TRAF2 and activates NF-κB, which causes the production of INFI and pro-inflammatory cytokines. Activated JNK and MAP kinases p38 at the downstream of ER stress responses also up-regulate cytokine production. eIF2: eukaryotic initiation factor 2; PERK: protein kinase R (PKR)-like ER kinase; IRE1: inositol-requiring enzymes; TRAF2: TNF receptor-associated factor 2; XBP1: X-box binding protein; ATF6, 4: activating transcription factor 6, 4; GRP78: glucose-regulated protein 78; IFN: interferon; TLR: toll-like receptor; RIG-1: retinoic acid-inducible gene-I-like receptor; NLR: nucleotide-binding oligomerization domain (NOD)-like receptor; GADD34: growth arrest and DNA damage inducible protein 34.