1. Lack of association between classical HLA genes and asymptomatic SARS-CoV-2 infection
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Marchal, A, Cirulli, E, Neveux, I, Bellos, E, Thwaites, R, Schiabor Barrett, K, Zhang, Y, Nemes-Bokun, I, Kalinova, M, Catchpole, A, Tangye, S, Spaan, A, Lack, J, Ghosn, J, Burdet, C, Gorochov, G, Tubach, F, Hausfater, P, Abel, L, Aiuti, A, Al-Muhsen, S, Al-Mulla, F, Amara, A, Anderson, M, Andreakos, E, Arias, A, Arkin, L, Feldman, H, Bastard, P, Belot, A, Biggs, C, Bogunovic, D, Bolze, A, Bondarenko, A, Borghesi, A, Bousfiha, A, Brodin, P, Bryceson, Y, Butte, M, Casanova, J, Casari, G, Christodoulou, J, Cobat, A, Colobran, R, Condino-Neto, A, Constantinescu, S, Cooper, M, Dalgard, C, Desai, M, Drolet, B, Duval, X, El Baghdadi, J, Eloy, P, Espinosa-Padilla, S, Fellay, J, Flores, C, Franco, J, Froidure, A, Gregersen, P, Grimbacher, B, Haerynck, F, Hagin, D, Halwani, R, Hammarstrom, L, Heath, J, Hsieh, E, Husebye, E, Imai, K, Itan, Y, Jouanguy, E, Kaja, E, Karamitros, T, Kisand, K, Ku, C, Lau, Y, Ling, Y, Lucas, C, Maniatis, T, Mansouri, D, Marodi, L, Mentre, F, Meyts, I, Milner, J, Mironska, K, Mogensen, T, Morio, T, Ng, L, Notarangelo, L, Novelli, A, Novelli, G, O'Farrelly, C, Okada, S, Okamoto, K, Ozcelik, T, Pan-Hammarstrom, Q, Pape, J, Perez de Diego, R, Perez-Tur, J, Perlin, D, Pesole, G, Planas, A, Prando, C, Pujol, A, Puel, A, Quintana-Murci, L, Ramaswamy, S, Renia, L, Resnick, I, Rodriguez-Gallego, C, Sancho-Shimizu, V, Sediva, A, Seppanen, M, Shahrooei, M, Shcherbina, A, Slaby, O, Snow, A, Soler-Palacin, P, Soumelis, V, Tancevski, I, Tayoun, A, Temel, S, Thorball, C, Tiberghien, P, Trouillet-Assant, S, Turvey, S, Uddin, K, Uddin, M, van de Beek, D, Vinh, D, von Bernuth, H, Wauters, J, Zatz, M, Zawadzki, P, Zhang, Q, Zhang, S, Bureau, S, Vacher, Y, Gysembergh-Houal, A, Demerville, L, Benleulmi-Chaachoua, A, Abad, S, Abassi, R, Abdellaoui, A, Abdelmalek, A, Abdoul, H, Abergel, H, Abeud, F, Abgrall, S, Abisror, N, Adechian, M, Aderdour, N, Admane, H, Adnet, F, Afritt, S, Agostini, H, Aguilar, C, Agut, S, Aiello, T, Kaci, M, Oufella, H, Ajeenthiravasan, G, 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- Abstract
Human genetic studies of critical COVID-19 pneumonia have revealed the essential role of type I interferon-dependent innate immunity to SARS-CoV-2 infection. Conversely, an association between the HLA-B∗15:01 allele and asymptomatic SARS-CoV-2 infection in unvaccinated individuals was recently reported, suggesting a contribution of pre-existing T cell-dependent adaptive immunity. We report a lack of association of classical HLA alleles, including HLA-B∗15:01, with pre-omicron asymptomatic SARS-CoV-2 infection in unvaccinated participants in a prospective population-based study in the United States (191 asymptomatic vs. 945 symptomatic COVID-19 cases). Moreover, we found no such association in the international COVID Human Genetic Effort cohort (206 asymptomatic vs. 574 mild or moderate COVID-19 cases and 1,625 severe or critical COVID-19 cases). Finally, in the Human Challenge Characterisation study, the three HLA-B∗15:01 individuals infected with SARS-CoV-2 developed symptoms. As with other acute primary infections studied, no classical HLA alleles favoring an asymptomatic course of SARS-CoV-2 infection were identified.
- Published
- 2024