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

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Published on: April 28, 2019

Subversion of interferon by dengue virus.

Jorge L Muñoz-Jordán¹

¹Division of Vector Borne Infectious Diseases, Dengue Branch, Centers for Disease Control and Prevention, 1324 Calle Cañada, San Juan, PR 00920, USA. ckq2@cdc.gov

Current Topics in Microbiology and Immunology

|October 6, 2009

Summary

Dengue virus evades the host

Area of Science:

Virology
Immunology
Molecular Biology

Background:

Mammalian cells detect dengue virus using Toll-like receptors and DExD/H box RNA helicases, initiating a Type 1 interferon response.
Interferon activates the JAK/STAT signaling pathway, leading to antiviral gene expression and cellular defense.
Dengue virus has evolved mechanisms to counteract this crucial interferon-mediated antiviral defense.

Purpose of the Study:

To investigate how dengue virus circumvents the host's interferon-mediated antiviral response.
To identify viral mechanisms that interfere with interferon signaling pathways.

Main Methods:

Analysis of dengue virus nonstructural proteins.
Investigating the impact of viral proteins on JAK/STAT pathway phosphorylation and gene expression.

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Utilizing replicon vectors to express viral components.

Main Results:

Dengue virus nonstructural proteins were found to inhibit the JAK/STAT signaling pathway.
Viral proteins reduce the phosphorylation of key JAK/STAT components.
This leads to decreased expression of interferon-stimulated genes, impairing the antiviral state.

Conclusions:

Dengue virus actively suppresses the host interferon response through its nonstructural proteins.
Understanding these viral evasion strategies is key to developing effective therapeutics.
This research opens avenues for improved biological models and drug discovery for dengue.