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Complement dysregulation is associated with severe COVID-19 illness.

Jia Yu1, Gloria F Gerber1, Hang Chen1

  • 1Division of Hematology, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, MD.

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Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) triggers complement system activation, leading to cell damage in COVID-19 patients. This complement dysregulation is linked to disease severity and may be a therapeutic target.

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Area of Science:

  • Immunology
  • Virology
  • Pathogenesis of Infectious Diseases

Background:

  • Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection can lead to severe complications including thrombosis and organ failure.
  • Complement system activation has been implicated in the pathogenesis of various diseases, including COVID-19.
  • Previous research indicated SARS-CoV-2 spike protein's role in activating the alternative pathway of complement (APC).

Purpose of the Study:

  • To investigate the role of complement activation in COVID-19 pathogenesis.
  • To assess the correlation between complement dysregulation and COVID-19 disease severity.
  • To explore the mechanism by which SARS-CoV-2 spike protein affects complement regulation.

Main Methods:

  • Functional assays (modified Ham test) were used to measure complement-mediated cell death induced by serum from 58 COVID-19 patients.
  • Membrane attack complex (C5b-9) deposition was assessed.
  • Inhibition of complement components (C5, Factor D) and measurement of Factor Bb levels were performed.
  • Interaction between SARS-CoV-2 spike protein and complement factor H was analyzed.

Main Results:

  • Serum from COVID-19 patients induced complement-mediated cell death and increased C5b-9 deposition.
  • A positive modified Ham assay was observed in 41.2% of intubated patients versus 6.3% of minimally oxygen-dependent patients.
  • Inhibition of C5 and Factor D reduced complement amplification; increased Factor Bb levels correlated with disease severity.
  • SARS-CoV-2 spike protein was shown to inhibit complement factor H binding to heparin.

Conclusions:

  • Complement dysregulation, particularly APC activation, contributes to COVID-19 pathogenesis.
  • Complement activation is associated with COVID-19 disease severity.
  • Targeting the complement system may offer a therapeutic strategy for COVID-19.