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C1 esterase inhibitor-mediated immunosuppression in COVID-19: Friend or foe?

Melissa A Hausburg1,2,3, Jason S Williams1,2,3, Kaysie L Banton1

  • 1Department of Trauma Research, Swedish Medical Center, 501 E. Hampden, Englewood, CO 80113, USA.

Clinical Immunology Communications
|November 28, 2023
PubMed

Insights

Severe COVID-19 involves aberrant complement and Factor XIIa activation. C1 esterase inhibitor (C1-INH) paradoxically increases, potentially inhibited by SARS-CoV-2, impacting immune responses.

Area of Science:

  • Immunology
  • Virology
  • Biochemistry

Background:

  • SARS-CoV-2 causes COVID-19 with varying severity, impacting innate and adaptive immunity.
  • Omicron variants reduce antibody neutralization, highlighting the need to understand immune responses.
  • Severe COVID-19 links to complement and Factor XIIa (FXIIa) overactivation.

Purpose of the Study:

  • To review C1 esterase inhibitor (C1-INH) roles in innate and adaptive immunity.
  • To explore C1-INH regulation by pathogens and SARS viruses.
  • To propose SARS-CoV-2 viral proteins inhibit C1-INH in severe COVID-19.

Main Methods:

  • Literature review of C1-INH function and regulation.
  • Analysis of C1-INH levels in COVID-19 patients.
  • Review of clinical trials on exogenous C1-INH treatment.

Main Results:

  • C1-INH, an inhibitor of complement and FXIIa, increases in COVID-19 patients.
  • Increased C1-INH correlates with disease severity.
  • Viral protein interaction with C1-INH is hypothesized to impair its function.

Conclusions:

  • C1-INH plays a complex role in COVID-19 pathogenesis.
  • Understanding C1-INH regulation is crucial for managing severe disease.
  • Exogenous C1-INH is being investigated as a potential therapeutic strategy.
Keywords:
C1 esterase inhibitorC1 esterase inhibitor, C1-INHC1-INHCOVID-19ComplementFXIIInflammationMiddle East respiratory syndrome coronavirus, MERS-CoVMycobacterium tuberculosis, MtbSevere acute respiratory syndrome coronavirus, SARS-CoVacquired C1-INH deficiency, AEEactivated plasma kallikrein, PKaantibody-mediated rejection, AMRbradykinin, BKcontact system, CScoronavirus disease 2019, COVID-19exogenous C1-INH, exC1-INHhereditary angioedema, HAEhigh-molecular-weight kininogen, HKhuman immunodeficiency virus, HIVinterferon, IFNinterleukin, ILischemia/reperfusion injury, IRImannose-binding lectin, MBLprekallikrein, PKrecombinant C1-INH, rhC1-INHserine protease inhibitor, serpintuberculosis, TB

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