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Hypoxia Exacerbates Inflammatory Signaling in Human Coronavirus OC43-Infected Lung Epithelial Cells
Jarod Zvartau-Hind1, Hassan Sadozai1, Hateem Z Kayani1
1Research Centre for Health & Life Sciences, University of Coventry, Coventry CV1 2DS, UK.
Biomolecules
|August 28, 2025
Summary
Hypoxia exacerbates inflammation in coronavirus infections, increasing the risk of severe COVID-19 complications. Targeting hypoxia signaling pathways may reduce harmful inflammatory responses.
Area of Science:
- * Molecular Biology
- * Immunology
- * Virology
Background:
- * Cytokine storm (CS) is linked to poor prognosis in COVID-19.
- * Hypoxic signaling may influence proinflammatory pathways and CS development.
- * The role of hypoxia in coronavirus-mediated inflammation requires investigation.
Purpose of the Study:
- * To investigate the role of hypoxia in coronavirus-induced inflammation.
- * To identify molecular changes in lung epithelial cells under combined hypoxia and HCoV-OC43 infection.
Main Methods:
- * Transcriptomic analysis using RNA sequencing on A549 lung epithelial cells.
- * Proteomic analysis of 105 cytokines and immune-related proteins using antibody arrays.
Main Results:
- * Combined hypoxia and HCoV-OC43 infection synergistically upregulated 191 mRNAs and downregulated 43 mRNAs.
- * Upregulated mRNAs were associated with inflammatory pathway activation.
- * Five proteins (IGFBP-3, VEGF, CCL20, CD30, myeloperoxidase) were markedly upregulated under hypoxia during HCoV-OC43 infection.
Conclusions:
- * COVID-19 patients with lung hypoxia may have a higher risk of inflammatory complications.
- * VEGF and CCL20 are potential therapeutic targets for reducing excessive inflammatory responses.
- * Inhibiting hypoxia signaling pathways could mitigate severe inflammatory cytokine responses.
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