Infectious Entry Of Dengue Virus Type 2 Into ECV304 Cells Occurs Through A Clathrin-mediated Endocytic Pathway

Dengue viruses (DV) are mosquito-borne RNA viruses, which belong to the genus Flavivirus (family Flaviviridae), and are grouped into four antigenically distinct types (DV-1, 2, 3, 4). DV is a causative agent for dengue fever (DF) and/or dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). Clinical manifestation of DHF/DSS is abrupt increased vascular permeability which leading to bleeding and shock. In addition to immunopathogenesis, interaction between virus and vascular endothelia cells (VEC) which result in dysfunction of VEC may mediate DHF/DSS. Therefore, defining how viruses interact with VEC is important for explaining the pathogenesis of DV and helpful for prevention and treatment of DHF/DSS.Initiation of a viral infection requires entry of the virus into the host cell, which is an early event and critical to the replication of virus. A virus particle proceeds through a multi-step entry process, involving interacting between components of virus and cells, during which each step is preprogrammed and tightly regulated in time and space. Virus can enter the cytoplasm directly at the cell surface, by penetrating the plasma membrane, or after endocytosis by penetrating membranes of intracellular organelles such as the endosome. The pathways of virus entry are cell type-dependent.Studying early virus-cell interactions will provide insights not only into the infectious cycle and thus into virus pathogenesis, but also into potential antiviral strategies. It is recognized that VEC is an important effective cell in DHF/DSS, and likewise is a target for DV replication in vivo; entry is an attractive target for inhibition because the entry machinery is extracellular and it is therefore easier for drug molecules to reach than intracellular targets. Consequently, the exploitation of the process and mechanism of DV enter VEC will benefit ours understanding of the mechanisms involving in virus-cell interaction and the pathogenesis of DV infection, and will take advantage of drug...