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Kachuri L, Francis SS, Morrison M, et al. The landscape of host genetic factors involved in immune response to common viral infections. medRxiv. 2020;doi: 10.1101/2020.05.01.20088054.
Kachuri, L., Francis, S. S., Morrison, M., Wendt, G. A., Bossé, Y., Cavazos, T. B., Rashkin, S. R., Ziv, E., & Witte, J. S. (2020). The landscape of host genetic factors involved in immune response to common viral infections. medRxiv : the preprint server for health sciences, . https://doi.org/10.1101/2020.05.01.20088054
Kachuri, Linda, et al. "The landscape of host genetic factors involved in immune response to common viral infections." medRxiv : the preprint server for health sciences vol. (2020). doi: https://doi.org/10.1101/2020.05.01.20088054
Kachuri L, Francis SS, Morrison M, Wendt GA, Bossé Y, Cavazos TB, Rashkin SR, Ziv E, Witte JS. The landscape of host genetic factors involved in immune response to common viral infections. medRxiv. 2020 Sep 05; doi: 10.1101/2020.05.01.20088054. PMID: 32511533; PMCID: PMC7273301.
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medRxiv. 2020 Sep 05; doi: 10.1101/2020.05.01.20088054.

The landscape of host genetic factors involved in immune response to common viral infections.

medRxiv : the preprint server for health sciences

Linda Kachuri, Stephen S Francis, Maike Morrison, George A Wendt, Yohan Bossé, Taylor B Cavazos, Sara R Rashkin, Elad Ziv, John S Witte

Affiliations

  1. Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, USA.
  2. Department of Neurological Surgery, University of California San Francisco, San Francisco, USA.
  3. Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, USA.
  4. Weill Institute for Neurosciences, University of California San Francisco, San Francisco, USA.
  5. Summer Research Training Program, Graduate Division, University of California San Francisco, San Francisco, USA.
  6. Department of Mathematics, The University of Texas at Austin, Austin, USA.
  7. Institut universitaire de cardiologie et de pneumologie de Québec, Department of Molecular Medicine, Université Laval, Quebec City, Canada.
  8. Program in Biological and Medical Informatics, University of California San Francisco, San Francisco, USA.
  9. Center for Applied Bioinformatics, St. Jude Children's Research Hospital, Memphis, USA.
  10. Department of Medicine, University of California, San Francisco, San Francisco, USA.
  11. Institute for Human Genetics, University of California San Francisco, San Francisco, USA.
  12. Department of Urology, University of California San Francisco, San Francisco, USA.

PMID: 32511533 PMCID: PMC7273301 DOI: 10.1101/2020.05.01.20088054

Abstract

INTRODUCTION: Humans and viruses have co-evolved for millennia resulting in a complex host genetic architecture. Understanding the genetic mechanisms of immune response to viral infection provides insight into disease etiology and therapeutic opportunities.

METHODS: We conducted a comprehensive study including genome-wide and transcriptome-wide association analyses to identify genetic loci associated with immunoglobulin G antibody response to 28 antigens for 16 viruses using serological data from 7924 European ancestry participants in the UK Biobank cohort.

RESULTS: Signals in human leukocyte antigen (HLA) class II region dominated the landscape of viral antibody response, with 40 independent loci and 14 independent classical alleles, 7 of which exhibited pleiotropic effects across viral families. We identified specific amino acid (AA) residues that are associated with seroreactivity, the strongest associations presented in a range of AA positions within DRβ1 at positions 11, 13, 71, and 74 for Epstein-Barr Virus (EBV), Varicella Zoster Virus (VZV), Human Herpes virus 7, (HHV7) and Merkel cell polyomavirus (MCV). Genome-wide association analyses discovered 7 novel genetic loci outside the HLA associated with viral antibody response (

CONCLUSIONS: Our study confirms the importance of the HLA region in host response to viral infection and elucidates novel genetic determinants beyond the HLA that contribute to host-virus interaction.

Keywords: Infection; antibody; antigen; genome-wide association study (GWAS); human leukocyte antigen (HLA); immune response; immunoglobulin G; polyomavirus; serology; transcriptome-wide association study (TWAS); virus

Conflict of interest statement

COMPETING INTERESTS The authors declare no competing interests.

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