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The **Dengue virus type 4 structural proteins** comprise three main viral proteins—*capsid (C)*, *precursor membrane/membrane (prM/M)*, and *envelope (E)*—that together form the architecture of the dengue virus particle[3][1]. The capsid protein organizes and packages the viral RNA genome inside the virion, the prM/M protein stabilizes the particle during assembly and maturation, and the E protein mediates receptor binding, viral entry, and fusion to host cells[3]. These proteins are essential for virus assembly, infectivity, and initiating infection in host cells. The structural proteins are considered important therapeutic and vaccine targets, especially the envelope protein, due to its central role in virus-host cell interactions and immunogenicity, though effective direct-acting drugs are currently lacking. Antibodies and vaccine candidates targeting these proteins can reduce infection but may contribute to antibody-dependent enhancement, a risk for dengue therapeutics and vaccines[3][1].
Inhibitors and antibodies: block viral entry, fusion, or assembly by binding to envelope (E) protein or prM Fusion inhibitors: prevent conformational changes in E needed for membrane fusion
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