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α2,6-Sialylation is Upregulated in Severe COVID-19 Implicating the Complement Cascade

Rui Qin1, Emma Kurz2, Shuhui Chen3

  • 1Department of Chemistry, University of Alberta, Edmonton, Alberta, Canada.

Medrxiv : the Preprint Server for Health Sciences
|June 15, 2022
PubMed

Insights

Severe COVID-19 involves hyper-inflammation. This study reveals increased alpha-2,6-sialylation and complement activation in severe cases, linking these processes to poor prognosis and fibrotic responses.

Area of Science:

  • Biochemistry
  • Immunology
  • Pathology

Background:

  • Understanding COVID-19 severity mechanisms is critical.
  • Hyper-inflammation is a hallmark of severe COVID-19, but triggers remain unclear.
  • The role of glycosylation in COVID-19 pathogenesis is unknown.

Approach:

  • First high-throughput glycomic analysis of COVID-19 plasma and autopsy tissues.
  • Investigated alpha-2,6-sialylation patterns in severe COVID-19.
  • Examined the relationship between sialylation, complement activation, and disease markers.

Key Points:

  • Alpha-2,6-sialylation is upregulated in plasma and lung tissue of severe COVID-19 patients.
  • This glycan motif is enriched on complement cascade members.
  • Increased sialylation correlates with complement deposition, IL-6, and fibrotic markers in lung tissue.
  • The ST6GAL1 enzyme is upregulated in fatal COVID-19 cases.

Conclusions:

  • Identified a novel link between sialylation and complement activation in severe COVID-19.
  • Findings suggest sialylation plays a role in COVID-19-associated hyper-inflammation and pathology.
  • This discovery may guide future therapeutic strategies for severe COVID-19.

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