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Updated: Jun 19, 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 pathogenesis: an integrated view.

Byron E E Martina¹, Penelope Koraka, Albert D M E Osterhaus

¹Erasmus Medical Center, Department of Virology, Rotterdam, The Netherlands. b.martina@erasmusmc.nl

Clinical Microbiology Reviews

|October 14, 2009

Summary

This summary is machine-generated.

Understanding dengue virus (DENV) pathogenesis is crucial. Research highlights viral factors and host responses in severe dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS), emphasizing personalized approaches for risk assessment.

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Area of Science:

Virology
Immunology
Pathogenesis

Background:

Dengue virus (DENV) infections manifest diversely, from mild to severe forms like dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS).
Cell and tissue tropism of DENV are key factors in disease development, necessitating better diagnostic tools and research models.
Extensive research suggests DHF and DSS pathogenesis involves viral virulence and host immune responses, leading to hemostasis issues and vascular leakage.

Purpose of the Study:

To explore the complex pathogenesis of DENV infections and their varied clinical outcomes.
To highlight the need for improved tropism assays, animal models, and human autopsy data for understanding DENV.
To investigate the mechanisms underlying severe dengue, including viral and host factors contributing to abnormal hemostasis and vascular permeability.

Main Methods:

Review of existing literature on DENV pathogenesis, viral tropism, and host responses.
Analysis of factors contributing to vascular hyperpermeability and hemostasis abnormalities in DHF and DSS.
Discussion of personalized approaches to study individual risk factors for severe dengue.

Main Results:

DENV pathogenesis is multifactorial, involving viral virulence and host immune responses.
Abnormal hemostasis and increased vascular permeability are hallmarks of severe dengue (DHF/DSS).
Targeting specific vascular beds may initiate localized hyperpermeability in DSS.

Conclusions:

Further research is needed to fully understand DENV pathogenesis and its clinical spectrum.
Personalized studies are essential to identify genetic and environmental factors influencing individual risk for severe dengue.
Developing better diagnostic tools and research models is critical for advancing dengue research.