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

Jérôme Hadjadj | Zendy; Nader Yatim | Zendy; Laura Barnabei | Zendy; Aurélien Corneau | Zendy; Jérémy Boussier | Zendy; Nikaïa Smith | Zendy; Hélène Péré | Zendy; Bruno Charbit | Zendy; Vincent Bondet | Zendy; Camille ChenevierGobeaux | Zendy; Paul Breillat | Zendy; Nicolas Carlier | Zendy; R. Gauzit | Zendy; Caroline Morbieu | Zendy; Frédéric Pène | Zendy; Nathalie Marin | Zendy; Nicolás Roche | Zendy; Tali-Anne Szwebel | Zendy; Sarah H. Merkling | Zendy; JeanMarc Tréluyer | Zendy; David Veyer | Zendy; Luc Mouthon | Zendy; Catherine Blanc | Zendy; PierreLouis Tharaux | Zendy; Flore Rozenberg | Zendy; Alain Fischer | Zendy; Darragh Duffy | Zendy; Frédéric RieuxLaucat | Zendy; Solen Kernéis | Zendy; Benjamin Terrier | Zendy

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

Author(s) -

Jérôme Hadjadj,

Nader Yatim,

Laura Barnabei,

Aurélien Corneau,

Jérémy Boussier,

Nikaïa Smith,

Hélène Péré,

Bruno Charbit,

Vincent Bondet,

Camille ChenevierGobeaux,

Paul Breillat,

Nicolas Carlier,

R. Gauzit,

Caroline Morbieu,

Frédéric Pène,

Nathalie Marin,

Nicolás Roche,

Tali-Anne Szwebel,

Sarah H. Merkling,

JeanMarc Tréluyer,

David Veyer,

Luc Mouthon,

Catherine Blanc,

PierreLouis Tharaux,

Flore Rozenberg,

Alain Fischer,

Darragh Duffy,

Frédéric RieuxLaucat,

Solen Kernéis,

Benjamin Terrier

Publication year - 2020

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.abc6027

Subject(s) - proinflammatory cytokine , immunology , interferon , biology , immune system , interferon type i , tumor necrosis factor alpha , lung , inflammation , immunity , virology , medicine

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.

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