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American Association for the Advancement of Science, Science, 6515(370), 2020

DOI: 10.1126/science.abd4570

American Academy of Pediatrics, Pediatrics, Supplement 3(148), p. S72-S73, 2021

DOI: 10.1542/peds.2021-053843bbbbb

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Inborn errors of type I IFN immunity in patients with life-threatening COVID-19

Journal article published in 2020 by Qian Zhang, Tom Le Voyer, Rui Yang, Qinhua Zhou, Saeed Al Turki, Aileen Camille Ugurbil, Zhiyong Liu, Peng Zhang, Marcela Moncada-Velez, Jie Chen, Franck Rapaport, S.-Y. Zhang, Masato Ogishi, B. Boisson, S. Boisson-Dupuis and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

The genetics underlying severe COVID-19 The immune system is complex and involves many genes, including those that encode cytokines known as interferons (IFNs). Individuals that lack specific IFNs can be more susceptible to infectious diseases. Furthermore, the autoantibody system dampens IFN response to prevent damage from pathogen-induced inflammation. Two studies now examine the likelihood that genetics affects the risk of severe coronavirus disease 2019 (COVID-19) through components of this system (see the Perspective by Beck and Aksentijevich). Q. Zhang et al. used a candidate gene approach and identified patients with severe COVID-19 who have mutations in genes involved in the regulation of type I and III IFN immunity. They found enrichment of these genes in patients and conclude that genetics may determine the clinical course of the infection. Bastard et al. identified individuals with high titers of neutralizing autoantibodies against type I IFN-α2 and IFN-ω in about 10% of patients with severe COVID-19 pneumonia. These autoantibodies were not found either in infected people who were asymptomatic or had milder phenotype or in healthy individuals. Together, these studies identify a means by which individuals at highest risk of life-threatening COVID-19 can be identified. Science , this issue p. eabd4570 , p. eabd4585 ; see also p. 404