Inherited and acquired errors of type I interferon immunity govern susceptibility to COVID-19 and multisystem inflammatory syndrome in children - 05/04/23
COVID Human Genetic Effort∗
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Abstract |
Since the beginning of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)/coronavirus disease 2019 (COVID-19) pandemic, global sequencing efforts have led in the field of inborn errors of immunity, and inspired particularly by previous research on life-threatening influenza, they have revealed that known and novel inborn errors affecting type I interferon immunity underlie critical COVID-19 in up to 5% of cases. In addition, neutralizing autoantibodies against type I interferons have been identified in up to 20% of patients with critical COVID-19 who are older than 80 years and 20% of fatal cases, with a higher prevalence in men and individuals older than 70 years. Also, inborn errors impairing regulation of type I interferon responses and RNA degradation have been found as causes of multisystem inflammatory syndrome in children, a life-threatening hyperinflammatory condition complicating otherwise mild initial SARS-CoV-2 infection in children and young adults. Better understanding of these immunologic mechanisms can aid in designing treatments for severe COVID-19, multisystem inflammatory syndrome in children, long COVID, and neuro-COVID.
Il testo completo di questo articolo è disponibile in PDF.Key words : COVID-19, SARS-CoV-2, multisystem inflammatory syndrome in children, type I interferon
Abbreviations used : ACE2, APS1, CGD, COVID-19, CYBB, dsRNA, HLH, IFNAR1/2, IFNLR1, IL-10RB, IRF9, MAVS, MIS-C, MYD88, NADPH, NLR, OAS, RIG-I, SARS-CoV-2, STAT, SOCS1, TLR, XIAP
Mappa
| Supported by the European Reference Network for Rare Immunodeficiency, Autoinflammatory and Autoimmune Diseases (ERN-RITA). I.M. is a senior clinical investigator at the Research Foundation–Flanders (FWO Vlaanderen) and is supported by a Katholieke Universiteit Leuven C1 (grant C16/18/007), the European Commission under Horizon Europe project UNDINE GA 10127100, the Research Foundation–Flanders (grants G0C8517N, G0B5120N, and G0E8420N), a European Research Council Starting Grant, and the Jeffrey Modell Foundation. H.C.S. and L.D.N. (listed under the COVID-Human Genetic Effort Consortium Consortium) are supported by the Division of Intramural Research of the National Institute of Allergy and Infectious Diseases, NIH. J.L.C. is supported by the National Institutes of Health (grants R01AI088364, R01AI163029, and UL1TR001866), Fisher Center for Alzheimer’s Research Foundation, Meyer Foundation, JPB Foundation, French National Research Agency (grants ANR-10-IAHU-01, ANR-10-LABX-62-IBEID, ANR-20-CE93-003, ANR-20-CO11-0001), French Foundation for Medical Research (grant EQU201903007798), ANRS-COV05, the European Union’s Horizon 2020 Research and Innovation Program (grant 824110; EASI-Genomics), HORIZON-HLTH-2021-DISEASE-04 Program (grant 01057100; UNDINE), the ANR-RHU COVIFERON Program (grant ANR-21-RHUS-08), the Square Foundation, Grandir-Fonds de solidarité pour l’enfance, the Fondation du Souffle, the SCOR Corporate Foundation for Science, and the French Ministry of Higher Education, Research, and Innovation (grant MESRI-COVID-19). |
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| Disclosure of potential conflict of interest: The authors declare that they have no conflicts of interest relevant to this manuscript. |
Vol 151 - N° 4
P. 832-840 - Aprile 2023 Ritorno al numero
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