Interindividual clinical variability in the course of SARS-CoV-2 infection is immense. We report that at least 101 of 987 patients with life-threatening COVID-19 pneumonia had neutralizing IgG auto-Abs against IFN-ω (13 patients), the 13 types of IFN-α (36), or both (52), at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1,227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 were men. A B cell auto-immune phenocopy of inborn errors of type I IFN immunity underlies life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men.

Clinical outcome upon infection with SARS-CoV-2 ranges from silent infection to lethal COVID-19. We have found an enrichment in rare variants predicted to be loss-of-function (LOF) at the 13 human loci known to govern TLR3- and IRF7-dependent type I interferon (IFN) immunity to influenza virus, in 659 patients with life-threatening COVID-19 pneumonia, relative to 534 subjects with asymptomatic or benign infection. By testing these and other rare variants at these 13 loci, we experimentally define LOF variants in 23 patients (3.5%), aged 17 to 77 years, underlying autosomal recessive or dominant deficiencies. We show that human fibroblasts with mutations affecting this pathway are vulnerable to SARS-CoV-2. Inborn errors of TLR3- and IRF7-dependent type I IFN immunity can underlie life-threatening COVID-19 pneumonia in patients with no prior severe infection.

Whole-exome sequencing reveals activating STAT1 mutations in some patients with autosomal dominant chronic mucocutaneous candidiasis disease.

Our results provide the basis for a detailed prospective evaluation of autoimmunity and inflammation in the context of PIDs, with a view to accurately assessing these risks and describing the possible effect of medical intervention.

The aim of the present study was to assess the food intakes and nutritional status of children with food allergies following an elimination diet. We conducted a cross sectional study including 96 children (mean age 4.7 ± 2.5 years) with food allergies and 95 paired controls (mean age 4.7 ± 2.7 years) without food allergies. Nutritional status was assessed using measurements of weight and height and Z scores for weight-for-age, height-for-age and weight-for-height. Nutrient intakes assessment was based on a 3-day diet record. Children with food allergies had weight-for-age and height-for-age Z scores lower than controls (0.1 versus 0.6 and 0.2 versus 0.8 respectively). Children with 3 or more food allergies were smaller than those with 2 or less food allergies (p = 0.04). A total of 62 children with food allergies and 52 controls completed usable diet records. Energy, protein and calcium intakes were similar in the two groups. Children with food allergies were smaller for their age than controls even when they received similar nutrient intakes. Nutritional evaluation is essential for the follow up of children with food allergies.