Abstract
Dengue is an old disease caused by the mosquito-borne dengue viruses (DENVs), which have four antigenically distinct serotypes (DENV1–4). Infection by any of them can cause dengue fever (DF) and/or a more serious disease, that is, dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS). In recent decades, incidence of dengue disease has increased 30-fold, putting a third to half of the world's population living in dengue-endemic areas at high infection risk. However, the pathogenesis of the disease is still poorly understood. The virus binding with its host cell is not only a first and critical step in their replication cycle but also a key factor for the pathogenicity. In recent years, there have been significant advances in understanding interactions of DENVs with their target cells such as dendritic cells (DC), macrophages, endothelial cells, and hepatocytes. Although DENVs reportedly attach to a variety of receptors on these cells, consensus DENV receptors have not been defined. In this review, we summarize receptors for DENVs on different cells identified in recent years.
Highlights
Dengue viruses (DENVs) belong to the Flaviviridae family
The single open reading frame is directly translated into a polyprotein precursor [1], which is subsequently glycosylated by cellular glycosyltransferases and cleaved by proteases from virus and host cell to release three structural proteins (envelope glycoprotein (E), membrane (M), and capsid (C)) and seven nonstructural proteins (NS1, NS2a, NS2b, NS3, NS4a, NS4b, and NS5)
There have been significant advances in understanding interactions of DENV with target cells such as dendritic cells (DCs), macrophages, vascular endothelial cells (VEC), and hepatocytes, and we would summarize receptors for DENVs on different cells identified in last several years in this review (Table 1)
Summary
Dengue viruses (DENVs) belong to the Flaviviridae family. Four antigenically distinct serotypes of the viruses (DENV1–4) are transmitted to humans through the mosquito vector, Aedes aegypti. According to reports of the World Health Organization (WHO), dengue disease is endemic in more than 100 countries in Africa, the Americas, the Eastern Mediterranean, Southeast Asia, and the Western Pacific. The single open reading frame is directly translated into a polyprotein precursor [1], which is subsequently glycosylated by cellular glycosyltransferases and cleaved by proteases from virus and host cell to release three structural proteins (envelope glycoprotein (E), membrane (M), and capsid (C)) and seven nonstructural proteins (NS1, NS2a, NS2b, NS3, NS4a, NS4b, and NS5). The DENVs enter the cells through receptor mediated endocytosis [4,5,6,7] and rearrange cell internal membranes to establish specific sites of replication [8,9,10]. There have been significant advances in understanding interactions of DENV with target cells such as dendritic cells (DCs), macrophages, vascular endothelial cells (VEC), and hepatocytes, and we would summarize receptors for DENVs on different cells identified in last several years in this review (Table 1)
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