Insufficient type I IFN immunity underlies life-threatening COVID-19 pneumonia

被引：10

作者：

Bastard, Paul ^{[1
,2
,3
]}

Zhang, Qian ^{[3
]}

Cobat, Aurelie ^{[1
,2
]}

Jouanguy, Emmanuelle ^{[1
,2
,3
]}

Zhang, Shen-Ying ^{[1
,2
,3
]}

Abel, Laurent ^{[1
,2
,3
]}

Casanova, Jean-Laurent ^{[1
,2
,3
,4
,5
]}

机构：

[1] Necker Hosp Sick Children, Necker Branch, Lab Human Genet Infect Dis, Inserm U1163, Paris, France

[2] Univ Paris, Imagine Inst, Paris, France

[3] Rockefeller Univ, St Giles Lab Human Genet Infect Dis, Rockefeller Branch, 1230 York Ave, New York, NY 10021 USA

[4] Howard Hughes Med Inst, New York, NY 10065 USA

[5] Inst Imagine, Lab Genet Humaine Malad Infect, INSERM U1163, 24 Bd Montparnasse, F-75015 Paris, France

来源：

COMPTES RENDUS BIOLOGIES | 2021年 / 344卷 / 01期

关键词：

Life-threatening COVID-19; Pneumonia; Type I interferons; Inborn errors of immunity; Autoantibodies; CHRONIC MUCOCUTANEOUS CANDIDIASIS; HERPES-SIMPLEX ENCEPHALITIS; AUTOANTIBODIES; SUSCEPTIBILITY; INFECTIONS; INTERFERON; DEFICIENCY; CHILDREN; PATIENT; GAMMA;

D O I：

10.5802/crbiol.36

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

We established the COVID Human Genetic Effort (www.covidhge.com) to discover the human genetic and immunological bases of the vast interindividual clinical variability between humans infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We found that about 3% of patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia were ill because of inborn errors of genes controlling type I interferon (IFN)-dependent immunity (which controls influenza virus), and at least 10% of patients with life-threatening COVID-19 pneumonia had neutralizing auto-Abs against some of the 17 individual type I IFNs. These findings indicate that impaired type I IFN immunity underlies life-threatening COVID-19 pneumonia in at least 13% of patients. These discoveries pave the way for further research into unexplained severe cases, and provide a rationale for preventing and treating the disease in individuals at risk, with recombinant type I IFNs.

引用

页码：19 / 25

页数：7

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