Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients.
Hadjadj J,Yatim N,Barnabei L,Corneau A,Boussier J,Smith N,Péré H,Charbit B,Bondet V,Chenevier-Gobeaux C,Breillat P,Carlier N,Gauzit R,Morbieu C,Pène F,Marin N,Roche N,Szwebel T,Merkling S,Treluyer J,Veyer D,Mouthon L,Blanc C,Tharaux P,Rozenberg F,Fischer A,Duffy D,Rieux-Laucat F,Kernéis S,Terrier B
Source :
Science
2020 Jul 13
Pmid / DOI:
32661059
Abstract
Coronavirus disease 2019 (COVID-19) is characterized by distinct patterns of disease progression that suggest diverse host immune responses. We performed an integrated immune analysis on a cohort of 50 COVID-19 patients with various disease severity. A distinct phenotype was observed in severe and critical patients, consisting of a highly impaired interferon (IFN) type I response (characterized by no IFN-β and low IFN-α production and activity), which was associated with a persistent blood viral load and an exacerbated inflammatory response. Inflammation was partially driven by the transcriptional factor nuclear factor-κB and characterized by increased tumor necrosis factor-α and interleukin-6 production and signaling. These data suggest that type I IFN deficiency in the blood could be a hallmark of severe COVID-19 and provide a rationale for combined therapeutic approaches.Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.