Dengue virus host cell receptor

Dengue virus host cell receptors are a group of structurally and functionally diverse molecules present on the surface of human and mosquito cells that facilitate the attachment and entry of dengue virus (DENV) into susceptible host cells. The primary viral attachment protein is the envelope (E) protein, which interacts with several types of host surface molecules. Candidate human receptors include sulfated glycosaminoglycans (such as heparan sulfate), lectins (such as DC-SIGN), glycosphingolipids (e.g., nLc4Cer), proteins with chaperone activity, and laminin-binding proteins[2][3]. In mosquitoes, distinct proteins in the salivary glands have been observed to bind DENV, but their detailed molecular identity remains undefined[1]. Following receptor engagement, the virus is internalized via endocytosis—primarily clathrin-mediated but also via macropinocytosis and other pathways depending on cell type and viral serotype[1]. Recognition of viral envelope phosphatidylserine (PS) by TIM and TAM family receptors can mediate macropinocytosis and play a role in immune evasion by mimicking apoptotic cell debris[1]. The broad range of host factors involved complicates therapeutic targeting. Some innate immune receptors, including Toll-like receptors (TLR3, TLR7), also contribute to sensing DENV and activating host defense, but are not strictly entry receptors[2]. Targeting host receptors is challenging due to their critical physiological functions and the risk of unwanted immunosuppression or enhanced viral infection[3][4]. Note: The entry "Dengue virus host cell receptors" is not a single molecule but a heterogeneous set; thus, it is not a canonical target and spans multiple molecular families. For structured data, it is advised to map to specific, characterized receptors (e.g., "Heparan sulfate", "DC-SIGN") where possible for drug discovery and biomarker applications[3].

Other names

Dengue virus entry receptorDENV receptorHost cell receptor for dengue virusDengue virus attachment factor

Blockade of virus-receptor interaction to prevent cell entry; Inhibition of endocytosis pathways critical for viral uptake; Neutralization by antibodies that prevent binding to cell receptors[3]