ArticleACS infectious diseases2022
α2,6-Sialylation Is Upregulated in Severe COVID-19, Implicating the Complement Cascade.
Article in ACS infectious diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Increased Mannosylation of Extracellular Vesicles in Long COVID Plasma as a Binding Target forInternational journal of molecular sciences · 2026Article
- Increased mannosylation of extracellular vesicles in Long COVID plasma provides a potential therapeutic target forbioRxiv : the preprint server for biology · 2025Article
- Glycosylation Variability of Serum α1-Acid Glycoprotein in the Context of Developing Inflammation and Oxidative Stress in Patients with Severe COVID-19.International journal of molecular sciences · 2025Article
- Lectin Microarray-based Glycomics and Machine Learning Identify Shared Osteoarthritis Biomarkers in Humans, Dogs, and Horses.bioRxiv : the preprint server for biology · 2025Article
- Integrated Multiomics Reveals Alterations in Paucimannose and Complex Type N-Glycans in Cardiac Tissue of Patients with COVID-19.Molecular & cellular proteomics : MCP · 2025Article
- Impact of different pathogen classes on the serumBBA advances · 2025Article
- Infection and the Glycome─New Insights into Host Response.ACS infectious diseases · 2024Review
- Deciphering disease through glycan codes: leveraging lectin microarrays for clinical insights.Acta biochimica et biophysica Sinica · 2024Review
- Total plasmaiScience · 2024Article
- IgM N-glycosylation correlates with COVID-19 severity and rate of complement deposition.Nature communications · 2024Article
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14 authors at 6 institutions in 2 countries.
Funding
Abstract
Better understanding of the molecular mechanisms underlying COVID-19 severity is desperately needed in current times. Although hyper-inflammation drives severe COVID-19, precise mechanisms triggering this cascade and what role glycosylation might play therein are unknown. Here we report the first high-throughput glycomic analysis of COVID-19 plasma samples and autopsy tissues. We find that α2,6-sialylation is upregulated in the plasma of patients with severe COVID-19 and in autopsied lung tissue. This glycan motif is enriched on members of the complement cascade (e.g., C5, C9), which show higher levels of sialylation in severe COVID-19. In the lung tissue, we observe increased complement deposition, associated with elevated α2,6-sialylation levels, corresponding to elevated markers of poor prognosis (IL-6) and fibrotic response. We also observe upregulation of the α2,6-sialylation enzyme ST6GAL1 in patients who succumbed to COVID-19. Our work identifies a heretofore undescribed relationship between sialylation and complement in severe COVID-19, potentially informing future therapeutic development.
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Registered trials
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