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Early Viral Entry Assays for the Identification and Evaluation of Antiviral Compounds
09:29

Early Viral Entry Assays for the Identification and Evaluation of Antiviral Compounds

Published on: October 29, 2015

Glycocalyx disruption mediates HP-PRRSV-induced microvascular endothelial dysfunction and underlies astragalus

Nuohan Xia1, Jian Sun2, Ge Hu1

  • 1Beijing Key Laboratory of Traditional Chinese Veterinary Medicine, Animal Science and Technology College, Beijing University of Agriculture, Beijing, China.

Open Veterinary Journal
|June 30, 2026
PubMed
Abstract

Insights

Astragalus polysaccharide (APS) protects pulmonary microvascular endothelial cells (MVECs) from highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) by maintaining glycocalyx integrity. Glycocalyx disruption worsens HP-PRRSV-induced lung injury, while APS treatment restores endothelial function.

Area of Science:

  • Veterinary Virology
  • Cell Biology
  • Immunology

Background:

  • Pulmonary microvascular endothelial cells (MVECs) are key targets and inflammatory hubs during highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) infection.
  • Glycocalyx disruption in MVECs initiates functional disorders, and astragalus polysaccharide (APS) is known to improve its integrity.

Purpose of the Study:

  • To investigate the role of glycocalyx disruption in HP-PRRSV-induced pulmonary microvascular endothelial dysfunction.
  • To determine the contribution of the glycocalyx to the therapeutic efficacy of APS against HP-PRRSV.

Main Methods:

  • HP-PRRSV infection of porcine pulmonary MVECs, treated with APS with or without prior glycocalyx degradation (heparinase III).
  • Analysis of glycocalyx components, viral protein, adhesion molecules, barrier function (TEER, HRP-SA permeability), and neutrophil function.
  • Detection methods included western blotting, flow cytometry, and Transwell assays.

Main Results:

  • HP-PRRSV infection reduced key glycocalyx components and induced endothelial dysfunction (decreased TEER, increased permeability, elevated adhesion molecules), and impaired neutrophil function.
  • APS treatment alleviated HP-PRRSV-induced damage, suppressed viral replication, and restored endothelial and neutrophil functions.
  • Enzymatic removal of the glycocalyx exacerbated injury and diminished APS efficacy.

Conclusions:

  • Glycocalyx disruption is a critical factor in HP-PRRSV-induced pulmonary microvascular endothelial dysfunction.
  • APS exerts therapeutic effects by preserving glycocalyx integrity and function, offering a novel therapeutic mechanism.
Keywords:
Astragalus polysaccharidesEndothelial dysfunctionGlycocalyxMicrovascular endothelial cellsPorcine reproductive and respiratory syndrome virus

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