Proteomic Profiling in Biracial Cohorts Implicates DC-SIGN as a Mediator of Genetic Risk in COVID-19

Daniel H. Katz, Usman A. Tahir, Debby Ngo, Mark Benson, Alexander G. Bick, Akhil Pampana, Yan Gao, Michelle J. Keyes, Adolfo Correa, Sumita Sinha, Dongxiao Shen, Qiong Yang, Jeremy M. Robbins, Zsu Zsu Chen, Daniel E. Cruz, Bennet Peterson, Pradeep Natarajan, Ramachandran S. Vasan, J. Gustav Smith, Thomas J. WangJames G. Wilson, Robert E. Gerszten

Research output: Contribution to journalArticlepeer-review

Abstract

COVID-19 is one of the most consequential pandemics in the last century, yet the biological mechanisms that confer disease risk are incompletely understood. Further, heterogeneity in disease outcomes is influenced by race, though the relative contributions of structural/social and genetic factors remain unclear.1,2 Very recent unpublished work has identified two genetic risk loci that confer greater risk for respiratory failure in COVID-19: the ABO locus and the 3p21.31 locus.3 To understand how these loci might confer risk and whether this differs by race, we utilized proteomic profiling and genetic information from three cohorts including black and white participants to identify proteins influenced by these loci. We observed that variants in the ABO locus are associated with levels of CD209/DC-SIGN, a known binding protein for SARS-CoV and other viruses,4 as well as multiple inflammatory and thrombotic proteins, while the 3p21.31 locus is associated with levels of CXCL16, a known inflammatory chemokine.5 Thus, integration of genetic information and proteomic profiling in biracial cohorts highlights putative mechanisms for genetic risk in COVID-19 disease.

Original languageEnglish (US)
JournalUnknown Journal
DOIs
StatePublished - Jun 11 2020

ASJC Scopus subject areas

  • Medicine(all)

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