Related Experiment Video

Updated: Sep 20, 2025

Screening for Functional Non-coding Genetic Variants Using Electrophoretic Mobility Shift Assay EMSA and DNA-affinity Precipitation Assay DAPA
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Screening for Functional Non-coding Genetic Variants Using Electrophoretic Mobility Shift Assay EMSA and DNA-affinity Precipitation Assay DAPA

Published on: August 21, 2016

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Shared genetic etiology and causality between COVID-19 and venous thromboembolism: evidence from genome-wide cross

Xin Huang, Minhao Yao, Peixin Tian

    Medrxiv : the Preprint Server for Health Sciences
    |June 6, 2022
    PubMed

    Insights

    Genetic links between COVID-19 and venous thromboembolism (VTE) were explored. Findings reveal shared genetic factors and a causal relationship, with VTE increasing COVID-19 risk and SARS-CoV-2 infection increasing VTE risk.

    Area of Science:

    • Genetics
    • Epidemiology
    • Immunology

    Background:

    • Venous thromboembolism (VTE) affects up to one-third of patients with COVID-19.
    • The shared genetic architecture between COVID-19 and VTE remains unclear.
    • Understanding this genetic overlap is crucial for managing VTE risk in COVID-19 patients.

    Approach:

    • Leveraged summary-level genetic data from the COVID-19 Host Genetics Consortium and UK Biobank.
    • Conducted cross-trait analysis to identify shared genetic loci between VTE and various COVID-19 traits (severe COVID-19, hospitalization, SARS-CoV-2 infection).
    • Utilized co-localization analysis and bi-directional Mendelian randomization to investigate causal relationships.

    Key Points:

    • Identified 8, 11, and 7 shared genetic loci between VTE and severe COVID-19, COVID-19 hospitalization, and SARS-CoV-2 infection, respectively.
    • Eight shared loci in genes like ABO, ADAMTS13, and FUT2 were confirmed through co-localization analysis.
    • Bi-directional Mendelian randomization indicated that VTE increases COVID-19 risk, and SARS-CoV-2 infection increases VTE risk.

    Conclusions:

    • Provided evidence for a shared genetic etiology between COVID-19 and VTE.
    • Established a causal link, suggesting VTE as a risk factor for COVID-19 and SARS-CoV-2 infection as a risk factor for VTE.
    • Highlighted the role of coagulation and immune function genes in the genetic overlap between these conditions.

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