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Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients

Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients
Jérôme Hadjadj #  1   2 , Nader Yatim #  2   3 , Laura Barnabei  1 , Aurélien Corneau  4 , Jeremy Boussier  3 , Nikaïa Smith  3 , Hélène Péré  5   6 , Bruno Charbit  7 , Vincent Bondet  3 , Camille Chenevier-Gobeaux  8 , Paul Breillat  2 , Nicolas Carlier  9 , Rémy Gauzit  10 , Caroline Morbieu  2 , Frédéric Pène  11   12 , Nathalie Marin  12 , Nicolas Roche  9   11 , Tali-Anne Szwebel  2 , Sarah H Merkling  13 , Jean-Marc Treluyer  14   15 , David Veyer  6   16 , Luc Mouthon  2   11 , Catherine Blanc  4 , Pierre-Louis Tharaux  5 , Flore Rozenberg  11   17 , Alain Fischer  1   18   19 , Darragh Duffy #  3   7 , Frédéric Rieux-Laucat #  1 , Solen Kernéis #  10   20   21 , Benjamin Terrier #  22   5

 

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.

 

Science. 2020 Aug 7;369(6504):718-724. doi: 10.1126/science.abc6027. Epub 2020 Jul 13.
PMID: 32661059 PMCID: PMC7402632
DOI: 10.1126/science.abc6027