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C1 esterase inhibitor and the contact system in COVID-19

Timothy M Thomson1,2, Emily Toscano-Guerra3, Ernesto Casis4

  • 1Barcelona Institute for Molecular Biology, National Science Council (IBMB-CSIC), Barcelona, Spain.

British Journal of Haematology
|June 13, 2020
PubMed

Insights

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection may cause a deficiency in C1 esterase inhibitor. This deficiency could explain serious systemic issues like vasculitis and hypercoagulation seen in COVID-19 patients.

Area of Science:

  • Immunology
  • Virology
  • Pathophysiology

Background:

  • Coronavirus disease 2019 (COVID-19) presents with severe systemic complications, including vasculitis, hyperinflammation, and hypercoagulation.
  • The underlying mechanisms for these critical COVID-19 manifestations are complex and multifactorial.

Purpose of the Study:

  • To investigate a potential pathogen-specific mechanism contributing to severe COVID-19 systemic abnormalities.
  • To explore the role of C1 esterase inhibitor deficiency in the pathophysiology of COVID-19.

Main Methods:

  • Analysis of publicly available protein-protein interaction networks (interactomes).
  • In silico investigation of potential molecular interactions between SARS-CoV-2 and host factors.

Main Results:

  • The study proposes that severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection directly leads to a deficiency in C1 esterase inhibitor.
  • This proposed deficiency is identified as a potential pathogen-specific mechanism.

Conclusions:

  • A SARS-CoV-2-induced deficiency in C1 esterase inhibitor may be a key factor explaining severe systemic abnormalities in COVID-19.
  • This finding offers a novel perspective on the hyperinflammatory and hypercoagulable states observed in patients with COVID-19.
Keywords:
SARS-CoV-2complementcontact systemserpinsvirology

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