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Arboviral Encephalitis

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...

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Updated: May 16, 2026

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease

Published on: April 28, 2019

Dengue virus type 2 modulates endothelial barrier function through CD73.

Chinmay Patkar, Kris Giaya, Daniel H Libraty

The American Journal of Tropical Medicine and Hygiene

|November 15, 2012

Summary

This summary is machine-generated.

Dengue hemorrhagic fever involves vascular leakage. Type I interferon-dependent CD73 up-regulation initially enhances endothelial barrier function in dengue virus type 2 (DENV2) infections, but later impairs recovery.

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Published on: May 5, 2023

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Last Updated: May 16, 2026

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease

Published on: April 28, 2019

Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis

Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis

Published on: May 5, 2023

Area of Science:

Virology
Immunology
Cell Biology

Background:

Dengue hemorrhagic fever presents with vascular leakage, but the underlying endothelial barrier dysfunction mechanisms remain unclear.
Understanding endothelial cell responses to dengue virus type 2 (DENV2) is crucial for addressing disease pathogenesis.

Purpose of the Study:

To investigate the role of endothelial barrier function modulation during DENV2 infection.
To elucidate the mechanisms of endothelial barrier dysfunction in dengue hemorrhagic fever.

Main Methods:

Primary human umbilical vein endothelial cells were infected with DENV2.
Endothelial barrier function was assessed over time.
The involvement of type I interferon signaling and CD73 expression was analyzed.

Main Results:

DENV2 infection initially increased endothelial barrier function within 72 hours, mediated by type I interferon-dependent CD73 up-regulation.
After 72 hours, DENV2 infection inhibited endothelial barrier recovery in response to TNF-α or VEGF.
This inhibition was linked to suppressed type I interferon receptor signaling and reduced CD73 levels.

Conclusions:

Endothelial barrier homeostasis in DENV2 infection is regulated by a balance of cytokines and type I interferon-dependent CD73.
CD73 plays a dual role in modulating endothelial barrier function during the course of DENV2 infection.