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SARS-CoV-2 triggers complement activation through interactions with heparan sulfate.

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Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) activates the complement system via the alternative pathway. This process involves heparan sulfate and leads to C5a production, impacting immune cell signaling.

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • The complement system is crucial for innate immunity.
  • SARS-CoV-2 infection can lead to severe inflammation.
  • Understanding SARS-CoV-2 interactions with the immune system is vital.

Purpose of the Study:

  • To investigate if SARS-CoV-2 triggers complement activation.
  • To identify the specific complement pathways involved.
  • To assess the functional consequences of SARS-CoV-2-induced complement activation.

Main Methods:

  • Utilized a human whole blood model with SARS-CoV-2.
  • Measured C5a production using ELISA.
  • Identified pathways with specific inhibitors and assessed C5a signaling markers via flow cytometry.

Main Results:

  • SARS-CoV-2 induced progressive C5a production over 24 hours.
  • Complement activation was inhibited by targeting factors B, C3, C5, and heparan sulfate.
  • Cell-free plasma experiments showed the necessity of cell surface interactions with heparan sulfate.
  • C5a receptor 1 (C5aR1) signaling and CD11b upregulation in leukocytes were delayed, occurring after 24 hours.

Conclusions:

  • SARS-CoV-2 acts as a noncanonical alternative pathway activator.
  • Complement activation is progressive and dependent on heparan sulfate interactions.
  • The study elucidates a novel mechanism of viral-induced complement activation.