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

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Hadjadj, Jérôme | Yatim, Nader | Barnabei, Laura | Corneau, Aurélien | Boussier, Jeremy | Smith, Nikaïa | Péré, Hélène | Charbit, Bruno | Bondet, Vincent | Chenevier-Gobeaux, Camille | Breillat, Paul | Carlier, Nicolas | Gauzit, Rémy | Morbieu, Caroline | Pène, Frédéric | Marin, Nathalie | Roche, Nicolas | Szwebel, Tali-Anne | Merkling, Sarah, Hélène | Treluyer, Jean-Marc | Veyer, David | Mouthon, Luc | Blanc, Catherine | Tharaux, Pierre-Louis | Rozenberg, Flore | Fischer, Alain | Duffy, Darragh | Rieux-Laucat, Frédéric | Kernéis, Solen | Terrier, Benjamin

Edité par CCSD ; American Association for the Advancement of Science (AAAS) -

International audience. Coronavirus disease 2019 (COVID-19) is characterized by distinct patterns of disease progression suggesting diverse host immune responses. We performed an integrated immune analysis on a cohort of 50 COVID-19 patients with various disease severity. A unique 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), associated with a persistent blood viral load and an exacerbated inflammatory response. Inflammation was partially driven by the transcriptional factor NF-κB and characterized by increased tumor necrosis factor (TNF)-α and interleukin (IL)-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.

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