Casanova, J.-L.Su, H. C.Abel, L.Aiuti, A.Almuhsen, S.Arias, A. A.Bastard, P.Biggs, C.Bogunovic, D.Boisson, B.Boisson-Dupuis, S.Bolze, A.Bondarenko, A.Bousfiha, A.Brodin, P.Bustamante, J.Butte, M.Casari, G.Ciancanelli, M.Cobat, A.Condino-Neto, A.Cooper, M.Dalgard, C.Espinosa, S.Feldman, H.Fellay, J.Franco, J. L.Hagin, D.Itan, Y.Jouanguy, E.Lucas, C.Mansouri, D.Meyts, I.Milner, J.Mogensen, T.Morio, T.Ng, L.Notarangelo, L. D.Okada, S.Özçelik, TayfunPalacín, P. S.Planas, A.Prando, C.Puel, A.Pujol, A.Redin, C.Renia, L.Gallego, J. C. R.Quintana-Murci, L.Sancho-Shimizu, V.Sankaran, V.Seppänen, M. R. J.Shahrooei, M.Snow, A.Spaan, A.Tangye, S.Tur, J. P.Turvey, S.Vinh, D. C.von Bernuth, H.Wang, X.Zawadzki, P.Zhang, Q.Zhang, S.2021-03-262021-03-2620200092-8674http://hdl.handle.net/11693/75984SARS-CoV-2 infection displays immense inter-individual clinical variability, ranging from silent infection to lethal disease. The role of human genetics in determining clinical response to the virus remains unclear. Studies of outliers—individuals remaining uninfected despite viral exposure and healthy young patients with life-threatening disease—present a unique opportunity to reveal human genetic determinants of infection and disease.EnglishArticle10.1016/j.cell.2020.05.016