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Updated: Oct 30, 2025

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Dengue and the Lectin Pathway of the Complement System
Romchat Kraivong1,2, Nuntaya Punyadee2,3, M Kathryn Liszewski4
1Molecular Biology of Dengue and Flaviviruses Research Team, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Bangkok 12120, Thailand.
The dengue virus (DENV) uses its surface N-glycans to evade immune responses. Mannan-binding lectin (MBL) neutralizes DENV, but the virus counteracts this through secreted nonstructural protein 1 (sNS1).
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Dengue virus (DENV) infection poses a global health and economic challenge, with severity influenced by serotype and prior exposure.
- The complement system, particularly the lectin pathway (LP), plays a dual role in dengue pathogenesis and protection.
- Foreign glycan recognition by lectin pattern recognition receptors (PRRs) is crucial for LP activation.
Purpose of the Study:
- To investigate the role of N-glycans on the DENV envelope in modulating lectin pathway activation and immune evasion.
- To elucidate the mechanisms by which mannan-binding lectin (MBL) neutralizes DENV and how DENV counteracts these effects.
Main Methods:
- Analysis of N-glycan structures on DENV envelope proteins.
- Assessment of MBL binding efficiency to different DENV glycoforms.
- Evaluation of complement activation-dependent and -independent neutralization mechanisms.
- Investigation of the role of DENV secreted nonstructural protein 1 (sNS1) in immune evasion.
Main Results:
- DENV N-glycans influence MBL binding and subsequent lectin pathway activation.
- MBL neutralizes DENV through direct glycan recognition and complement-mediated opsonization.
- DENV sNS1 antagonizes MBL activity, promoting viral survival and dissemination.
- Serum concentrations and polymorphisms of lectin PRRs impact LP-mediated dengue immunity.
Conclusions:
- DENV N-glycan variations are key determinants of host immune interactions.
- MBL-mediated neutralization is a critical host defense mechanism against DENV.
- DENV sNS1 represents a significant viral evasion strategy, highlighting a complex interplay between virus and host immunity.
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