SARS-CoV-2 spike protein interacts with and activates TLR4

We here identified that the trimeric spike protein of SARS-CoV-2 could bind to TLR4 directly and robustly activate downstream signaling in monocytes and neutrophils. Moreover, specific TLR4 or NFKB inhibitor, or knockout of MyD88 could significantly block IL-1B induction by spike protein. We thus reveal that spike protein of SARS-CoV-2 functions as a potent stimulus causing TLR4 activation and sepsis related abnormal responses. Overall design: RNAseq analysis of THP-1 cells with SARS-CoV-2 Spike protein or LPS stimuli.