Abstract
Dengue virus (DENV) infections are expanding worldwide and, because of the lack of a vaccine, the search for antiviral products is imperative. Four serotypes of DENV are described and they all cause a similar disease outcome. It would be interesting to develop an antiviral product that can interact with all four serotypes, prevent host cell infection and subsequent immune activation. DENV entry is thus an interesting target for antiviral therapy. DENV enters the host cell through receptor-mediated endocytosis. Several cellular receptors have been proposed, and DC-SIGN, present on dendritic cells, is considered as the most important DENV receptor until now. Because DENV entry is a target for antiviral therapy, various classes of compounds have been investigated to inhibit this process. In this paper, an overview is given of all the putative DENV receptors, and the most promising DENV entry inhibitors are discussed.
Highlights
Dengue virus (DENV) is a single-stranded, positive-sense enveloped RNA virus of the Flaviviridae family that is transmitted by Aedes aegypti and Aedes albopictus
Diagnosis is largely clinical, treatment is supportive through hydration, and disease control is limited by eradication of the mosquito
The search for cellular receptors responsible for DENV capture leads to the identification of cell-surface C-type lectin dendritic cells (DCs)-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN; CD209) [34, 35, 61, 77]
Summary
Dengue virus (DENV) is a single-stranded, positive-sense enveloped RNA virus of the Flaviviridae family that is transmitted by Aedes aegypti and Aedes albopictus. It is proposed that viral epitopes on the surface of DENV can trigger cellular immune responses and subsequently the development of a severe disease. These epitopes are potential targets for the development of a new class of antiviral products, DENV entry inhibitors. The cellular immune response is believed to play an important role in antibody-dependent enhancement (ADE). This is a phenomenon where crossreacting nonneutralizing antibodies generated to the first DENV infection will recognize a heterologous DENV during a secondary infection with another serotype. Specific molecules preventing the interaction between the host and DENV envelope are discussed
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