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Causal relationships between interleukins, interferons and COVID-19 risk: a Mendelian randomization study
Chao Wang1, Xin Wang2, Sainan Zhang1
1College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang, China.
International Journal of Environmental Health Research
|September 3, 2023
Summary
This Mendelian randomization study reveals specific interleukins (ILs) and interferons (IFNs) that causally influence COVID-19 risk. Certain ILs and IFNs decrease risk, while others increase it, offering potential therapeutic targets.
Area of Science:
- Immunology
- Genetics
- Infectious Diseases
Background:
- Observational studies suggest associations between COVID-19 risk and cytokines like interleukins (ILs) and interferons (IFNs).
- The precise causal relationships between specific ILs, IFNs, and COVID-19 remain unclear.
Purpose of the Study:
- To investigate the causal effects of 47 cytokines, including 35 ILs and 12 IFNs, on COVID-19 risk.
- To elucidate the genetic underpinnings of cytokine involvement in COVID-19 pathogenesis.
Main Methods:
- Mendelian randomization analysis utilizing single nucleotide polymorphisms (SNPs) as instrumental variables (IVs).
- Employed three methods for causal effect estimation and MR-Egger regression for horizontal pleiotropy assessment.
- Conducted sensitivity analyses to ensure the robustness of the findings.
Main Results:
- Identified six cytokines associated with decreased COVID-19 risk: Interferon-omega-1 (IFN-W1) and Interleukins (IL-5, IL-6, IL-13, IL-16, IL-37).
- Identified six cytokines associated with increased COVID-19 risk: Interferon-gamma (IFNG) and Interleukins (IL-3, IL-8, IL-27, IL-31, IL-36β).
Conclusions:
- This Mendelian randomization study establishes causal links between specific ILs, IFNs, and COVID-19 risk.
- Findings provide valuable insights into potential cytokine-targeted therapeutic strategies for managing COVID-19.
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