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Related Experiment Video

Updated: Jan 9, 2026

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Dengue Virus NS1 Binds Ephrin B1 to Trigger Endothelial Dysfunction.

Felix Pahmeier1,2, Sabrina R Hammond1, Charlotte Flory3

  • 1Division of Infectious Diseases and Vaccinology, School of Public Health, University of California, Berkeley, Berkeley, CA, USA.

Biorxiv : the Preprint Server for Biology
|December 3, 2025
PubMed
Summary

Dengue virus (DENV) non-structural protein 1 (NS1) causes vascular leak by interacting with host factor ephrin B1 (EFNB1). Blocking this interaction with EFNB1-Fc decoys prevents DENV-induced barrier dysfunction.

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Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Dengue virus (DENV) is a significant mosquito-borne pathogen.
  • DENV non-structural protein 1 (NS1) induces vascular leak by affecting endothelial cells.
  • The host factors mediating NS1-induced endothelial dysfunction are not fully understood.

Purpose of the Study:

  • To investigate the host interactome of DENV NS1 in endothelial cells.
  • To identify host factors critical for NS1-mediated endothelial barrier dysfunction.
  • To explore potential therapeutic strategies targeting the NS1-host interaction.

Main Methods:

  • Comparative mass spectrometry to identify host interactors of DENV NS1.
  • Biochemical and computational approaches to map the EFNB1-NS1 complex interface.
  • In vitro and in vivo assays using EFNB1-Fc fusion proteins as decoys.

Main Results:

  • Ephrin B1 (EFNB1) was identified as a critical host factor in NS1-induced endothelial barrier dysfunction.
  • Phosphorylation of EFNB1 is essential for NS1-mediated barrier dysfunction.
  • EFNB1-Fc fusion proteins effectively blocked NS1-induced vascular leak in vitro and in vivo.

Conclusions:

  • EFNB1 is a key host factor mediating DENV NS1-induced endothelial barrier dysfunction.
  • Targeting the EFNB1-NS1 interaction with decoy proteins offers a potential therapeutic strategy against dengue.
  • This study elucidates a mechanism of flavivirus-induced vascular leak and suggests novel therapeutic avenues.