Frontiers in Immunology (Jul 2021)
Individual HLA-A, -B, -C, and -DRB1 Genotypes Are No Major Factors Which Determine COVID-19 Severity
- Johannes Schetelig,
- Johannes Schetelig,
- Falk Heidenreich,
- Falk Heidenreich,
- Henning Baldauf,
- Sarah Trost,
- Bose Falk,
- Christian Hoßbach,
- Ruben Real,
- Axel Roers,
- Dirk Lindemann,
- Alexander Dalpke,
- Martin Kolditz,
- Katja de With,
- Martin Bornhäuser,
- Ezio E. Bonifacio,
- Elke Rücker-Braun,
- Elke Rücker-Braun,
- Vinzenz Lange,
- Jan Markert,
- Ralf Barth,
- Jan A. Hofmann,
- Jürgen Sauter,
- Stefanie N. Bernas,
- Alexander H. Schmidt,
- Alexander H. Schmidt,
- Alexander H. Schmidt
Affiliations
- Johannes Schetelig
- Clinical Trials Unit, DKMS, Dresden, Germany
- Johannes Schetelig
- Division of Hematology, Department of Internal Medicine I, University Hospital Carl Gustav Carus, Technische Universität (TU), Dresden, Dresden, Germany
- Falk Heidenreich
- Clinical Trials Unit, DKMS, Dresden, Germany
- Falk Heidenreich
- Division of Hematology, Department of Internal Medicine I, University Hospital Carl Gustav Carus, Technische Universität (TU), Dresden, Dresden, Germany
- Henning Baldauf
- Clinical Trials Unit, DKMS, Dresden, Germany
- Sarah Trost
- Clinical Trials Unit, DKMS, Dresden, Germany
- Bose Falk
- Clinical Trials Unit, DKMS, Dresden, Germany
- Christian Hoßbach
- Clinical Trials Unit, DKMS, Dresden, Germany
- Ruben Real
- Clinical Trials Unit, DKMS, Dresden, Germany
- Axel Roers
- Institute for Immunology, TU Dresden, Dresden, Germany
- Dirk Lindemann
- Institute of Medical Microbiology and Virology, University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany
- Alexander Dalpke
- Institute of Medical Microbiology and Virology, University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany
- Martin Kolditz
- Division of Pulmonology, Department of Internal Medicine I, University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany
- Katja de With
- Division of Infectious Diseases, TU Dresden, Dresden, Germany
- Martin Bornhäuser
- Division of Hematology, Department of Internal Medicine I, University Hospital Carl Gustav Carus, Technische Universität (TU), Dresden, Dresden, Germany
- Ezio E. Bonifacio
- Center for Regenerative Therapies Dresden (CRTD), TU Dresden, Dresden, Germany
- Elke Rücker-Braun
- Clinical Trials Unit, DKMS, Dresden, Germany
- Elke Rücker-Braun
- Division of Hematology, Department of Internal Medicine I, University Hospital Carl Gustav Carus, Technische Universität (TU), Dresden, Dresden, Germany
- Vinzenz Lange
- DKMS Life Science Lab, Dresden, Germany
- Jan Markert
- DKMS, Stem Cell Donor Registry, Tübingen, Germany
- Ralf Barth
- DKMS, Stem Cell Donor Registry, Tübingen, Germany
- Jan A. Hofmann
- DKMS, Stem Cell Donor Registry, Tübingen, Germany
- Jürgen Sauter
- DKMS, Stem Cell Donor Registry, Tübingen, Germany
- Stefanie N. Bernas
- DKMS, Stem Cell Donor Registry, Tübingen, Germany
- Alexander H. Schmidt
- Clinical Trials Unit, DKMS, Dresden, Germany
- Alexander H. Schmidt
- DKMS Life Science Lab, Dresden, Germany
- Alexander H. Schmidt
- DKMS, Stem Cell Donor Registry, Tübingen, Germany
- DOI
- https://doi.org/10.3389/fimmu.2021.698193
- Journal volume & issue
-
Vol. 12
Abstract
HLA molecules are key restrictive elements to present intracellular antigens at the crossroads of an effective T-cell response against SARS-CoV-2. To determine the impact of the HLA genotype on the severity of SARS-CoV-2 courses, we investigated data from 6,919 infected individuals. HLA-A, -B, and -DRB1 allotypes grouped into HLA supertypes by functional or predicted structural similarities of the peptide-binding grooves did not predict COVID-19 severity. Further, we did not observe a heterozygote advantage or a benefit from HLA diplotypes with more divergent physicochemical peptide-binding properties. Finally, numbers of in silico predicted viral T-cell epitopes did not correlate with the severity of SARS-CoV-2 infections. These findings suggest that the HLA genotype is no major factor determining COVID-19 severity. Moreover, our data suggest that the spike glycoprotein alone may allow for abundant T-cell epitopes to mount robust T-cell responses not limited by the HLA genotype.
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