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. 2022 Jun 27;13:948770. doi: 10.3389/fmicb.2022.948770

FIGURE 1.

FIGURE 1

Toll-like receptor-mediated antiviral and inflammatory responses during SARS-CoV-2 infection. TLR1/2/6 and 4 localize to cell membrane, and TLR3, TLR7/8, and 9 localize to endosome surface. The viral proteins of SARS-CoV-2 signal through TLR2 and TLR4 to activate the adaptor MyD88, which subsequently signals via NF-κB and MAPK to promote the expression of proinflammatory cytokines. TLR4 also recruits the adapter protein TRIF, which activates the TRAF3, resulting the IRF3 activation to lead the production of type I and III IFN. The ssRNA or dsRNA replication intermediates of SARS-CoV-2 are recognized by TLR3 and TLR7/8, respectively. The TLR7/8 recruit MyD88, and TLR3 via TRIF molecule. The proinflammatory cytokines induced by DAMPs accumulating during SARS-CoV-2 infection are driven by the transcription factor NF-κB. MAL, MyD88 adapter-like; TRAF, tumor necrosis factor receptor-associated factor; TRIF, TIR-domain-containing adapter-inducing interferon-β; TRAM, TRIF-related adaptor molecule; IRAK1/4, interleukin-1 receptor associated kinase 1/4; TAK1, transforming growth factor β-activated kinase 1; TAB, TAK1-binding proteins; IKK, IkB kinase; TBK1, TANK-binding kinase 1; ERK1/2, extracellular signal-regulated kinases 1/2; JNK, c-Jun N-terminal kinase; AP-1, activating protein-1.