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Updated: May 14, 2026

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Carbohydrate-related inhibitors of dengue virus entry
Kazuya I P J Hidari1, Tomoko Abe, Takashi Suzuki
1Department of Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, and Global COE Program for Innovation in Human Health Sciences, 52-1 Yada, Suruga-ku, Shizuoka-shi, Shizuoka 422-8526, Japan. hidari@u-shizuoka-ken.ac.jp
Abstract:
Dengue virus (DENV), which is transmitted by Aedes mosquitoes, causes fever and hemorrhagic disorders in humans. The virus entry process mediated through host receptor molecule(s) is crucial for virus propagation and the pathological progression of dengue disease. Therefore, elucidation of the molecular mechanisms underlying virus entry is essential for an understanding of dengue pathology and for the development of effective new anti-dengue agents. DENV binds to its receptor molecules mediated through a viral envelope (E) protein, followed by incorporation of the virus-receptor complex inside cells. The fusion between incorporated virus particles and host endosome membrane under acidic conditions is mediated through the function of DENV E protein. Carbohydrate molecules, such as sulfated glycosaminoglycans (GAG) and glycosphingolipids, and carbohydrate-recognition proteins, termed lectins, inhibit virus entry. This review focuses on carbohydrate-derived entry inhibitors, and also introduces functionally related compounds with similar inhibitory mechanisms against DENV entry.
Insights
Carbohydrate-based compounds can block dengue virus (DENV) entry into human cells by interfering with its envelope protein. These findings offer potential for developing new dengue fever treatments.
Area of Science:
- Virology
- Molecular Biology
- Biochemistry
Background:
- Dengue virus (DENV) causes significant human illness, including fever and hemorrhagic disorders.
- Virus entry into host cells, mediated by the viral envelope (E) protein and host receptors, is critical for DENV propagation and disease.
- Understanding DENV entry mechanisms is key to developing antiviral therapies.
Purpose of the Study:
- To review carbohydrate-derived molecules that inhibit DENV entry.
- To explore compounds with similar mechanisms of action against DENV entry.
Main Methods:
- Focus on the role of the DENV envelope (E) protein in receptor binding and membrane fusion.
- Investigate the inhibitory effects of carbohydrate molecules like sulfated glycosaminoglycans (GAGs) and glycosphingolipids.
- Examine the function of lectins (carbohydrate-recognition proteins) in blocking DENV entry.
Main Results:
- Carbohydrate molecules and lectins demonstrate inhibitory effects on DENV entry.
- The DENV E protein mediates virus-receptor binding and subsequent fusion within endosomes.
- Specific carbohydrate structures and their interactions with viral proteins are crucial for inhibition.
Conclusions:
- Carbohydrate-derived compounds represent a promising strategy for developing novel anti-dengue agents.
- Targeting the DENV entry process offers a viable therapeutic approach.
- Further research into these inhibitors could lead to effective dengue treatments.
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