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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 06748naa a2201645 4500 | |
| 001 | oai:prod.swepub.kib.ki.se:236324795 | |
| 003 | SwePub | |
| 008 | 240811s2022 | |||||||||||000 ||eng| | |
| 024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:2363247952 URI |
| 024 | 7 | a https://doi.org/10.1101/2022.10.22.222812212 DOI |
| 040 | a (SwePub)ki | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a vet2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Matuozzo, D4 aut |
| 245 | 1 0 | a Rare predicted loss-of-function variants of type I IFN immunity genes are associated with life-threatening COVID-19 |
| 264 | 1 | b Cold Spring Harbor Laboratory,c 2022 |
| 520 | a BackgroundWe previously reported inborn errors of TLR3- and TLR7-dependent type I interferon (IFN) immunity in 1-5% of unvaccinated patients with life-threatening COVID-19, and auto-antibodies against type I IFN in another 15-20% of cases.MethodsWe report here a genome-wide rare variant burden association analysis in 3,269 unvaccinated patients with life-threatening COVID-19 (1,301 previously reported and 1,968 new patients), and 1,373 unvaccinated SARS-CoV-2-infected individuals without pneumonia. A quarter of the patients tested had antibodies against type I IFN (234 of 928) and were excluded from the analysis.ResultsNo gene reached genome-wide significance. Under a recessive model, the most significant gene with at-risk variants wasTLR7, with an OR of 27.68 (95%CI:1.5-528.7,P=1.1×10−4), in analyses restricted to biochemically loss-of-function (bLOF) variants. We replicated the enrichment in rare predicted LOF (pLOF) variants at 13 influenza susceptibility loci involved in TLR3-dependent type I IFN immunity (OR=3.70 [95%CI:1.3-8.2],P=2.1×10−4). Adding the recently reportedTYK2COVID-19 locus strengthened this enrichment, particularly under a recessive model (OR=19.65 [95%CI:2.1-2635.4];P=3.4×10−3). When these 14 loci andTLR7were considered, all individuals hemizygous (n=20) or homozygous (n=5) for pLOF or bLOF variants were patients (OR=39.19 [95%CI:5.2-5037.0],P=4.7×10−7), who also showed an enrichment in heterozygous variants (OR=2.36 [95%CI:1.0-5.9],P=0.02). Finally, the patients with pLOF or bLOF variants at these 15 loci were significantly younger (mean age [SD]=43.3 [20.3] years) than the other patients (56.0 [17.3] years;P=1.68×10−5).ConclusionsRare variants of TLR3- and TLR7-dependent type I IFN immunity genes can underlie life-threatening COVID-19, particularly with recessive inheritance, in patients under 60 years old. | |
| 700 | 1 | a Talouarn, E4 aut |
| 700 | 1 | a Marchal, A4 aut |
| 700 | 1 | a Manry, J4 aut |
| 700 | 1 | a Seeleuthner, Y4 aut |
| 700 | 1 | a Zhang, Y4 aut |
| 700 | 1 | a Bolze, A4 aut |
| 700 | 1 | a Chaldebas, M4 aut |
| 700 | 1 | a Milisavljevic, B4 aut |
| 700 | 1 | a Zhang, P4 aut |
| 700 | 1 | a Gervais, A4 aut |
| 700 | 1 | a Bastard, P4 aut |
| 700 | 1 | a Asano, T4 aut |
| 700 | 1 | a Bizien, L4 aut |
| 700 | 1 | a Barzaghi, F4 aut |
| 700 | 1 | a Abolhassani, Hu Karolinska Institutet4 aut |
| 700 | 1 | a Tayoun, AA4 aut |
| 700 | 1 | a Aiuti, A4 aut |
| 700 | 1 | a Darazam, IA4 aut |
| 700 | 1 | a Allende, LM4 aut |
| 700 | 1 | a Alonso-Arias, R4 aut |
| 700 | 1 | a Arias, AA4 aut |
| 700 | 1 | a Aytekin, G4 aut |
| 700 | 1 | a Bergman, P4 aut |
| 700 | 1 | a Bondesan, S4 aut |
| 700 | 1 | a Bryceson, YT4 aut |
| 700 | 1 | a Bustos, IG4 aut |
| 700 | 1 | a Cabrera-Marante, O4 aut |
| 700 | 1 | a Carcel, S4 aut |
| 700 | 1 | a Carrera, P4 aut |
| 700 | 1 | a Casari, G4 aut |
| 700 | 1 | a Chaïbi, K4 aut |
| 700 | 1 | a Colobran, R4 aut |
| 700 | 1 | a Condino-Neto, A4 aut |
| 700 | 1 | a Covill, LE4 aut |
| 700 | 1 | a El Zein, L4 aut |
| 700 | 1 | a Flores, C4 aut |
| 700 | 1 | a Gregersen, PK4 aut |
| 700 | 1 | a Gut, M4 aut |
| 700 | 1 | a Haerynck, F4 aut |
| 700 | 1 | a Halwani, R4 aut |
| 700 | 1 | a Hancerli, S4 aut |
| 700 | 1 | a Hammarström, L4 aut |
| 700 | 1 | a Hatipoğlu, N4 aut |
| 700 | 1 | a Karbuz, A4 aut |
| 700 | 1 | a Keles, S4 aut |
| 700 | 1 | a Kyheng, C4 aut |
| 700 | 1 | a Leon-Lopez, R4 aut |
| 700 | 1 | a Franco, JL4 aut |
| 700 | 1 | a Mansouri, D4 aut |
| 700 | 1 | a Martinez-Picado, J4 aut |
| 700 | 1 | a Akcan, OM4 aut |
| 700 | 1 | a Migeotte, I4 aut |
| 700 | 1 | a Morange, PE4 aut |
| 700 | 1 | a Morelle, G4 aut |
| 700 | 1 | a Martin-Nalda, A4 aut |
| 700 | 1 | a Novelli, G4 aut |
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| 700 | 1 | a Ozcelik, T4 aut |
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| 700 | 1 | a Sobh, A4 aut |
| 700 | 1 | a Soler-Palacin, P4 aut |
| 700 | 1 | a Tandjaoui-Lambiotte, Y4 aut |
| 700 | 1 | a Tipu, I4 aut |
| 700 | 1 | a Tresoldi, C4 aut |
| 700 | 1 | a Troya, J4 aut |
| 700 | 1 | a van de Beek, D4 aut |
| 700 | 1 | a Zatz, M4 aut |
| 700 | 1 | a Zawadzki, P4 aut |
| 700 | 1 | a Al-Muhsen, SZ4 aut |
| 700 | 1 | a Baris-Feldman, H4 aut |
| 700 | 1 | a Butte, MJ4 aut |
| 700 | 1 | a Constantinescu, SN4 aut |
| 700 | 1 | a Cooper, MA4 aut |
| 700 | 1 | a Dalgard, CL4 aut |
| 700 | 1 | a Fellay, J4 aut |
| 700 | 1 | a Heath, JR4 aut |
| 700 | 1 | a Lau, YL4 aut |
| 700 | 1 | a Lifton, RP4 aut |
| 700 | 1 | a Maniatis, T4 aut |
| 700 | 1 | a Mogensen, TH4 aut |
| 700 | 1 | a von Bernuth, H4 aut |
| 700 | 1 | a Lermine, A4 aut |
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| 700 | 1 | a Hausfater, P4 aut |
| 700 | 1 | a Meyts, I4 aut |
| 700 | 1 | a Zhang, SY4 aut |
| 700 | 1 | a Puel, A4 aut |
| 700 | 1 | a Notarangelo, LD4 aut |
| 700 | 1 | a Boisson-Dupuis, S4 aut |
| 700 | 1 | a Su, HC4 aut |
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| 700 | 1 | a Jouanguy, E4 aut |
| 700 | 1 | a Casanova, JL4 aut |
| 700 | 1 | a Zhang, Q4 aut |
| 700 | 1 | a Abel, L4 aut |
| 700 | 1 | a Cobat, A4 aut |
| 710 | 2 | a Karolinska Institutet4 org |
| 773 | 0 | t medRxiv : the preprint server for health sciencesd : Cold Spring Harbor Laboratory |
| 856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:236324795 |
| 856 | 4 8 | u https://doi.org/10.1101/2022.10.22.22281221 |
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- Hammarström, L
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