About: Impaired type I interferon activity and exacerbated inflammatory responses in severe Covid-19 patients

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About: Impaired type I interferon activity and exacerbated inflammatory responses in severe Covid-19 patients Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Impaired type I interferon activity and exacerbated inflammatory responses in severe Covid-19 patients
Creator	Mouthon, Luc Rozenberg, Flore Morbieu, Caroline Chenevier-Gobeaux, Camille Barnabei, Laura Blanc, Catherine Bondet, Vincent Boussier, Jeremy Breillat, Paul Carlier, Nicolas Charbit, Bruno Corneau, Aurélien Duffy, Darragh Fischer, Alain Gauzit, Rémy Hadjadj, Jérôme Kernéis, Solen Marin, Nathalie Merkling, Sarah Pène, Frédéric Péré, Hélène Rieux-Laucat, Frédéric Roche, Nicolas Smith, Nikaïa Szwebel, Tali-Anne Tharaux, Pierre-Louis Treluyer, Jean-Marc Yatim, Nader Verer, David
Source	MedRxiv
abstract	Background: Coronavirus disease 2019 (Covid-19) is a major global threat that has already caused more than 100,000 deaths worldwide. It is characterized by distinct patterns of disease progression implying a diverse host immune response. However, the immunological features and molecular mechanisms involved in Covid-19 severity remain so far poorly known. Methods: We performed an integrated immune analysis that included in-depth phenotypical profiling of immune cells, whole-blood transcriptomic and cytokine quantification on a cohort of fifty Covid19 patients with a spectrum of disease severity. All patient were tested 8 to 12 days following first symptoms and in absence of anti-inflammatory therapy. Results: A unique phenotype in severe and critically ill patients was identified. It consists in a profoundly impaired interferon (IFN) type I response characterized by a low interferon production and activity, with consequent downregulation of interferon-stimulated genes. This was associated with a persistent blood virus load and an exacerbated inflammatory response that was partially driven by the transcriptional factor NFκB. It was also characterized by increased tumor necrosis factor (TNF)-α and interleukin (IL)-6 production and signaling as well as increased innate immune chemokines. Conclusion: We propose that type-I IFN deficiency in the blood is a hallmark of severe Covid-19 and could identify and define a high-risk population. Our study provides a rationale for testing IFN administration combined with adapted anti-inflammatory therapy targeting IL-6 or TNF-α in most severe patients. These data also raise concern for utilization of drugs that interfere with the IFN pathway.
has issue date	2020-04-23(xsd:dateTime)
bibo:doi	10.1101/2020.04.19.20068015
has license	medrxiv
sha1sum (hex)	fc5150277fa072b2e602e5fdf301c4962b033936
schema:url	https://doi.org/10.1101/2020.04.19.20068015
resource representing a document's title	Impaired type I interferon activity and exacerbated inflammatory responses in severe Covid-19 patients
resource representing a document's body	covid:fc5150277fa072b2e602e5fdf301c4962b033936#body_text
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