tetano
Editor, Senior Moderator
Science
. 2020 Jul 13;eabc6027.
doi: 10.1126/science.abc6027. Online ahead of print.
Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients
J?r?me Hadjadj[SUP] #[/SUP][SUP] 1 2 [/SUP], Nader Yatim[SUP] #[/SUP][SUP] 2 3 [/SUP], Laura Barnabei[SUP] 1 [/SUP], Aur?lien Corneau[SUP] 4 [/SUP], Jeremy Boussier[SUP] 3 [/SUP], Nika?a Smith[SUP] 3 [/SUP], H?l?ne P?r?[SUP] 5 6 [/SUP], Bruno Charbit[SUP] 7 [/SUP], Vincent Bondet[SUP] 3 [/SUP], Camille Chenevier-Gobeaux[SUP] 8 [/SUP], Paul Breillat[SUP] 2 [/SUP], Nicolas Carlier[SUP] 9 [/SUP], R?my Gauzit[SUP] 10 [/SUP], Caroline Morbieu[SUP] 2 [/SUP], Fr?d?ric P?ne[SUP] 11 [/SUP], Nathalie Marin[SUP] 11 [/SUP], Nicolas Roche[SUP] 9 [/SUP], Tali-Anne Szwebel[SUP] 2 [/SUP], Sarah H Merkling[SUP] 12 [/SUP], Jean-Marc Treluyer[SUP] 13 [/SUP], David Veyer[SUP] 5 [/SUP], Luc Mouthon[SUP] 2 [/SUP], Catherine Blanc[SUP] 4 [/SUP], Pierre-Louis Tharaux[SUP] 6 [/SUP], Flore Rozenberg[SUP] 14 [/SUP], Alain Fischer[SUP] 1 15 16 [/SUP], Darragh Duffy[SUP] #[/SUP][SUP] 3 7 [/SUP], Fr?d?ric Rieux-Laucat[SUP] #[/SUP][SUP] 1 [/SUP], Solen Kern?is[SUP] #[/SUP][SUP] 10 17 [/SUP], Benjamin Terrier[SUP] #[/SUP][SUP] 18 6 [/SUP]
Affiliations
Abstract
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.
. 2020 Jul 13;eabc6027.
doi: 10.1126/science.abc6027. Online ahead of print.
Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients
J?r?me Hadjadj[SUP] #[/SUP][SUP] 1 2 [/SUP], Nader Yatim[SUP] #[/SUP][SUP] 2 3 [/SUP], Laura Barnabei[SUP] 1 [/SUP], Aur?lien Corneau[SUP] 4 [/SUP], Jeremy Boussier[SUP] 3 [/SUP], Nika?a Smith[SUP] 3 [/SUP], H?l?ne P?r?[SUP] 5 6 [/SUP], Bruno Charbit[SUP] 7 [/SUP], Vincent Bondet[SUP] 3 [/SUP], Camille Chenevier-Gobeaux[SUP] 8 [/SUP], Paul Breillat[SUP] 2 [/SUP], Nicolas Carlier[SUP] 9 [/SUP], R?my Gauzit[SUP] 10 [/SUP], Caroline Morbieu[SUP] 2 [/SUP], Fr?d?ric P?ne[SUP] 11 [/SUP], Nathalie Marin[SUP] 11 [/SUP], Nicolas Roche[SUP] 9 [/SUP], Tali-Anne Szwebel[SUP] 2 [/SUP], Sarah H Merkling[SUP] 12 [/SUP], Jean-Marc Treluyer[SUP] 13 [/SUP], David Veyer[SUP] 5 [/SUP], Luc Mouthon[SUP] 2 [/SUP], Catherine Blanc[SUP] 4 [/SUP], Pierre-Louis Tharaux[SUP] 6 [/SUP], Flore Rozenberg[SUP] 14 [/SUP], Alain Fischer[SUP] 1 15 16 [/SUP], Darragh Duffy[SUP] #[/SUP][SUP] 3 7 [/SUP], Fr?d?ric Rieux-Laucat[SUP] #[/SUP][SUP] 1 [/SUP], Solen Kern?is[SUP] #[/SUP][SUP] 10 17 [/SUP], Benjamin Terrier[SUP] #[/SUP][SUP] 18 6 [/SUP]
Affiliations
- PMID: 32661059
- DOI: 10.1126/science.abc6027
Abstract
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.