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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 hemorrhage in a mouse model.

Betty A Wu-Hsieh¹, Yu-Ting Yen, Hsuen-Chin Chen

¹National Taiwan University, College of Medicine, Graduate Institute of Immunology, Taipei, Taiwan. bwh@ntu.edu.tw

Annals of the New York Academy of Sciences

|September 16, 2009

Summary

Dengue virus (DENV) infection causes hemorrhage in mice by damaging endothelial cells. Reactive oxygen and nitrogen species (ROS/RNS) contribute to this damage, offering targets for new dengue treatments.

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Area of Science:

Virology
Immunology
Pathology

Background:

Dengue hemorrhage is a severe complication of DENV infection.
The precise mechanisms leading to hemorrhage remain incompletely understood.

Purpose of the Study:

To investigate the pathological events leading to dengue hemorrhage using a mouse model.
To elucidate the role of reactive oxygen and nitrogen species (ROS/RNS) in DENV-induced hemorrhage.

Main Methods:

Immunocompetent mice were intradermally inoculated with DENV-2.
Hemorrhage incidence and severity were correlated with viral inoculum size.
Analysis of endothelial damage, thrombocytopenia, bleeding time, and macrophage infiltration.
Assessment of iNOS, peroxynitrite, apoptosis, and the effects of iNOS deficiency, phox47 deficiency, and apocynin treatment.

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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

A Murine Model of Subarachnoid Hemorrhage

A Murine Model of Subarachnoid Hemorrhage

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Main Results:

DENV-2 infection in mice resulted in local or systemic hemorrhage, dependent on viral inoculum.
Hemorrhagic mice exhibited thrombocytopenia, prolonged bleeding, and increased circulating endothelial cells.
Endothelial damage, macrophage infiltration, TNF-alpha secretion, iNOS expression, peroxynitrite formation, and apoptosis were observed.
ROS and RNS were demonstrated to be critical factors in hemorrhage development.

Conclusions:

A mouse model for dengue hemorrhage was established, revealing the roles of endothelial damage and ROS/RNS.
ROS/RNS production contributes significantly to DENV-induced hemorrhage.
This model can be utilized for evaluating dengue vaccines, therapeutics, and viral strain pathogenicity.