Journal
AMERICAN JOURNAL OF HUMAN GENETICS
Volume 97, Issue 5, Pages 738-743Publisher
CELL PRESS
DOI: 10.1016/j.ajhg.2015.09.008
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Funding
- Max Planck Society
- Max Planck Forderstiftung
- DFG Research Center for Nanoscale Microscopy and Molecular Physiology of the Brain
- Niedersachsen-Research Network on Neuroinfectiology of the Ministry of Science and Culture of Lower Saxony
- Brain & Behavior Research Foundation
- Daimler and Benz Foundation
- Swiss National Science Foundation [PP00P3_133703]
- Swiss National Science Foundation (SNF) [PP00P3_133703] Funding Source: Swiss National Science Foundation (SNF)
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The magnitude of the human antibody response to viral antigens is highly variable. To explore the human genetic contribution to this variability, we performed genome-wide association studies of the immunoglobulin G response to 14 pathogenic viruses in 2,363 immunocompetent adults. Significant associations were observed in the major histocompatibility complex region on chromosome 6 for influenza A virus, Epstein-Barr virus, JC polyomavirus, and Merkel cell polyomavirus. Using local imputation and fine mapping, we identified specific amino acid residues in human leucocyte antigen (HLA) class II proteins as the most probable causal variants underlying these association signals. Common HLA-DR beta 1 haplotypes showed virus-specific patterns of humoral-response regulation. We observed an overlap between variants affecting the humoral response to influenza A and EBV and variants previously associated with autoimmune diseases related to these viruses. The results of this study emphasize the central and pathogen-specific role of HLA class II variation in the modulation of humoral immune response to viral antigens in humans.
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