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Local Complement Contributes to Pathogenic Activation of Lung Endothelial Cells in SARS-CoV-2 Infection.

Hui Zhang1, Evgenia Gerasimovskaya1, Mary K McCarthy2

  • 1Cardiovascular Pulmonary Research Laboratories, Department of Pediatrics and Medicine.

American Journal of Respiratory Cell and Molecular Biology
|April 18, 2023
PubMed
Summary

COVID-19 vascular issues stem from inflammation, not direct viral infection of endothelial cells. Lung vascular cells show low susceptibility to SARS-CoV-2, but inflammation and complement activation occur, contributing to COVID-19 vascular pathology.

Keywords:
coronavirus disease (COVID-19)extracellular ATPhypoxiainflammationlung microvascular endothelial cells

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Area of Science:

  • Vascular Biology
  • Infectious Diseases
  • Immunology

Background:

  • Endothelial dysfunction and inflammation are key in COVID-19 vascular pathology.
  • Direct SARS-CoV-2 infection of vascular cells is not supported by evidence, suggesting inflammation is a secondary response.

Purpose of the Study:

  • To investigate SARS-CoV-2 susceptibility in lung vascular cells.
  • To determine the role of complement activation in endothelial dysfunction during COVID-19.

Main Methods:

  • Compared ACE2 and TMPRSS2 mRNA expression in lung vascular vs. epithelial cells.
  • Assessed SARS-CoV-2 infection in primary human lung microvascular endothelial cells (HLMVECs) under normoxic and hypoxic conditions.
  • Analyzed inflammatory and complement factor expression in HLMVECs exposed to conditioned medium from infected epithelial cells and hypoxia.

Main Results:

  • Lung vascular cells express significantly lower ACE2 and TMPRSS2 mRNA than alveolar epithelial cells.
  • HLMVECs are not productively infected by SARS-CoV-2, though abortive infection occurs.
  • Exposure to infected epithelial cell medium and hypoxia upregulates inflammatory markers (ICAM-1, VCAM-1, IL-6) and complement components (C3, C3AR1, C1QA, CFB) in HLMVECs.

Conclusions:

  • Lung endothelial and vascular dysfunction in COVID-19 is linked to complement activation and inflammatory signaling.
  • Productive SARS-CoV-2 infection of endothelial cells is not the cause of COVID-19 vascular pathology.