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Updated: May 30, 2026
04:23
A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Exploitation of cellular pathways by Dengue virus.
Wolfgang Fischl1, Ralf Bartenschlager
1Department of Infectious Diseases, Molecular Virology, Heidelberg University, Im Neuenheimer Feld 345, 69120 Heidelberg, Germany.
Current Opinion in Microbiology
|July 30, 2011
Summary
Dengue virus (DENV) exploits host cell pathways like ER-associated degradation and autophagy for replication. Understanding these DENV-host interactions is key to developing effective antiviral therapies against this global health threat.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Dengue virus (DENV) causes a significant global health burden as the most prevalent arthropod-borne viral disease.
- DENV has a limited coding capacity, necessitating the exploitation of host cell machinery for its replication.
Purpose of the Study:
- To elucidate the intricate interactions between DENV and host cell components.
- To identify host cell pathways crucial for efficient DENV replication.
- To understand viral strategies against host innate antiviral responses.
Main Methods:
- Investigated host cell pathways utilized by DENV.
- Analyzed the role of ER-associated degradation, autophagy, unfolded protein response, and lipid droplets in DENV replication.
- Examined viral mechanisms to counteract host antiviral defenses.
Main Results:
- Identified ER-associated degradation, autophagy, unfolded protein response, and lipid droplets as critical for DENV replication.
- Unraveled specific strategies employed by DENV to overcome host innate immunity.
Conclusions:
- The DENV-host cell relationship is complex, involving significant viral manipulation of cellular processes.
- Further understanding of these interactions is essential for designing novel antiviral strategies against dengue.
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