Journal
VIRUSES-BASEL
Volume 5, Issue 2, Pages 605-618Publisher
MDPI AG
DOI: 10.3390/v5020605
Keywords
dengue virus; receptor; endocytosis; fusion; entry inhibitor; carbohydrate; glycosaminoglycan
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Funding
- Ministry of Education, Science, Sports, and Culture of Japan [21570146, 24570168]
- Cooperative Research Grant of the Institute of Tropical Medicine, Nagasaki University [2010-A-7]
- Heiwa Nakajima Foundation
- Japan China Medical Association
- Grants-in-Aid for Scientific Research [25460126, 21570146, 24570168] Funding Source: KAKEN
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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.
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