@article{Marchal:2024:10.1016/j.xhgg.2024.100300,
author = {Marchal, A and Cirulli, ET and Neveux, I and Bellos, E and Thwaites, RS and Schiabor, Barrett KM and Zhang, Y and Nemes-Bokun, I and Kalinova, M and Catchpole, A and Tangye, SG and Spaan, AN and Lack, JB and Ghosn, J and Burdet, C and Gorochov, G and Tubach, F and Hausfater, P and COVID, Human Genetic Effort and COVIDeF, Study Group and French, COVID Cohort Study Group and CoV-Contact, Cohort and COVID-STORM, Clinicians and COVID, Clinicians and Orchestra, Working Group and Amsterdam, UMC COVID-19 Biobank and NIAID-USUHS, COVID Study Group and Dalgard, CL and Zhang, S-Y and Zhang, Q and Chiu, C and Fellay, J and Grzymski, JJ and Sancho-Shimizu, V and Abel, L and Casanova, J-L and Cobat, A and Bolze, A},
doi = {10.1016/j.xhgg.2024.100300},
journal = {HGG Advances},
title = {Lack of association between classical HLA genes and asymptomatic SARS-CoV-2 infection},
url = {http://dx.doi.org/10.1016/j.xhgg.2024.100300},
volume = {5},
year = {2024}
}

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TY  - JOUR
AB  - 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.
AU  - Marchal,A
AU  - Cirulli,ET
AU  - Neveux,I
AU  - Bellos,E
AU  - Thwaites,RS
AU  - Schiabor,Barrett KM
AU  - Zhang,Y
AU  - Nemes-Bokun,I
AU  - Kalinova,M
AU  - Catchpole,A
AU  - Tangye,SG
AU  - Spaan,AN
AU  - Lack,JB
AU  - Ghosn,J
AU  - Burdet,C
AU  - Gorochov,G
AU  - Tubach,F
AU  - Hausfater,P
AU  - COVID,Human Genetic Effort
AU  - COVIDeF,Study Group
AU  - French,COVID Cohort Study Group
AU  - CoV-Contact,Cohort
AU  - COVID-STORM,Clinicians
AU  - COVID,Clinicians
AU  - Orchestra,Working Group
AU  - Amsterdam,UMC COVID-19 Biobank
AU  - NIAID-USUHS,COVID Study Group
AU  - Dalgard,CL
AU  - Zhang,S-Y
AU  - Zhang,Q
AU  - Chiu,C
AU  - Fellay,J
AU  - Grzymski,JJ
AU  - Sancho-Shimizu,V
AU  - Abel,L
AU  - Casanova,J-L
AU  - Cobat,A
AU  - Bolze,A
DO  - 10.1016/j.xhgg.2024.100300
PY  - 2024///
SN  - 2666-2477
TI  - Lack of association between classical HLA genes and asymptomatic SARS-CoV-2 infection
T2  - HGG Advances
UR  - http://dx.doi.org/10.1016/j.xhgg.2024.100300
UR  - https://www.ncbi.nlm.nih.gov/pubmed/38678364
UR  - https://www.sciencedirect.com/science/article/pii/S2666247724000393?via%3Dihub
UR  - http://hdl.handle.net/10044/1/112752
VL  - 5
ER  - 

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