The SARS-CoV-2 spike protein primes inflammasome-mediated interleukin-1- beta secretion in COVID-19 patient-derived macrophages (preprint)

Innate immunity triggers responsible for viral control or hyperinflammation in COVID- 19 are largely unknown. Here we show that the SARS-CoV-2 spike protein primes inflammasome activation and interleukin 1-beta (IL-1β) secretion in macrophages derived from COVID-19 patients but not in macrophages from healthy SARS-CoV-2 naïve controls. Chemical NLRP3 inhibition blocks spike protein-induced IL-1β secretion ex vivo. These findings can accelerate research on COVID-19 vaccine design and drug treatment.