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TBEV NS1 Induces Tissue-Specific Microvascular Endothelial Cell Permeability by Activating the TNF-α Signaling

Yana Khlusevich1, Bogdana Kravchuk1, Andrey Kechin1

  • 1Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of Russian Academy of Sciences, 630090 Novosibirsk, Russia.

International Journal of Molecular Sciences
|June 13, 2025
PubMed
Summary

Tick-borne encephalitis virus (TBEV) NS1 protein increases human lung endothelial cell permeability. This occurs by activating inflammatory pathways, highlighting a new aspect of TBEV pathogenesis.

Keywords:
NS1 proteinTEERTNF-α signaling pathwayendothelial hyperpermeabilityflavivirustick-borne encephalitis virus

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Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Tick-borne encephalitis virus (TBEV) causes severe neurological disease.
  • The role of flavivirus NS1 proteins in endothelial permeability is known, but TBEV NS1 is understudied.

Purpose of the Study:

  • To investigate the effect of TBEV NS1 on human endothelial cell permeability.
  • To identify the signaling pathways involved in TBEV NS1-induced endothelial dysfunction.

Main Methods:

  • Recombinant TBEV NS1 protein produced in eukaryotic cells was used.
  • Human endothelial permeability was assessed using TEER and transwell assays.
  • Signaling pathways were analyzed using RNA sequencing.

Main Results:

  • TBEV NS1 directly affected human lung microvascular endothelial cells (HLMVECs) in vitro.
  • TBEV NS1 did not affect human umbilical vein endothelial cells (HUVECs).
  • TBEV NS1 induced hyperpermeability in HLMVECs by activating TNF-α and inflammatory signaling.

Conclusions:

  • TBEV NS1 protein contributes to endothelial hyperpermeability in specific human cell types.
  • Activation of TNF-α and inflammatory pathways is a key mechanism for TBEV NS1-induced endothelial dysfunction.
  • This study provides novel insights into TBEV pathogenesis at the endothelial level.