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Dengue virus non-structural protein 1 activates the p38 MAPK pathway to decrease barrier integrity in primary human

Arturo Barbachano-Guerrero1, Timothy P Endy1, Christine A King1

  • 1Department of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse NY, USA.

The Journal of General Virology
|March 7, 2020
PubMed
Summary
This summary is machine-generated.

Dengue virus non-structural protein 1 (NS1) activates endothelial cells, causing vascular leakage. This occurs via the p38 MAPK pathway, contributing to severe dengue pathogenesis.

Keywords:
Dengue virusendothelial cellflavivirusp38 MAPKvascular permeability

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Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Dengue virus (DENV) causes millions of infections globally, with severe forms characterized by vascular leakage.
  • Endothelial cells (ECs) maintain vascular homeostasis but are not typically infected by DENV.
  • DENV non-structural protein 1 (NS1) is secreted and implicated in vascular permeability, though the mechanism is unclear.

Purpose of the Study:

  • To investigate the effect of DENV NS1 on human endothelial cells (ECs).
  • To elucidate the molecular mechanism by which NS1 impacts EC barrier function and homeostasis.

Main Methods:

  • Primary human ECs were treated with DENV NS1.
  • Confocal microscopy, transcriptomic analysis, and trans-endothelial electrical resistance (TEER) assays were performed.
  • Western blotting (WB) assessed the p38 MAPK pathway activation.

Main Results:

  • NS1 was rapidly internalized by ECs, altering functions related to homeostasis and permeability.
  • NS1 induced a rapid, transient loss of EC barrier function within 3 hours.
  • NS1 activated the p38 MAPK pathway and its downstream effectors, which was reversed by p38 MAPK inhibition.

Conclusions:

  • DENV NS1 activates the p38 MAPK pathway in ECs.
  • This activation leads to increased EC permeability, contributing to the vascular leakage seen in severe dengue.