Dengue hemorrhagic fever is a life-threatening disease caused by the dengue virus (DENV). After DENV enters into host cells, it replicates to generate viral particles to infect other cells. DENV exploits components of the cellular trafficking pathway to achieve effective virion production. Understanding of the proteins required for this trafficking process is essential for revealing the pathogenesis of DENV infection. Coat protein complex and soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs), two host protein families in the cellular trafficking pathway, were investigated to elucidate their respective roles during DENV infection. Coat proteins (COPI and COPII) and SNAREs (STX 5 and NSF) were knocked down in a DENV-infected Huh7 cells by RNA interference. Depletion of COPI and COPII, but not of STX5 and NSF, decreased DENV production in DENV-infected Huh7 cells. DENV proteins, including DENV C, prM, E, and NS1, were significantly reduced in COPI-silenced DENV-infected Huh7 cells, when compared to those of control cells. COPI also facilitated DENV production in an endothelial cell line and in all DENV serotypes, indicating the importance of coat protein complex in facilitating DENV infection.
Keywords: COPI; Dengue virus; Replication; SNAREs; Virion production.
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