Dengue virus serotype 2 cellular entry receptor (None established; DENV-2 entry receptor is sometimes used informally.)

The term “DENV-2 cellular entry receptors” refers to the diverse set of host cell surface molecules that mediate the attachment and entry of dengue virus serotype 2 (DENV-2) into human cells. Unlike other viruses that use a single, highly specific receptor, DENV-2 exploits several proteins to facilitate internalization, often in a cell-type–specific manner. Key receptors and attachment factors include C-type lectin family proteins such as DC-SIGN (on dendritic cells), the mannose receptor (in monocytes/macrophages), and the TIM and TAM family of phosphatidylserine receptors (utilized via apoptotic mimicry)[1][2][3]. Fc gamma receptors also mediate viral uptake under conditions of antibody-dependent enhancement (ADE). Heparan sulfate proteoglycans, langerin, and other factors may contribute to viral binding in other cell types. DENV-2 entry typically proceeds via clathrin-mediated endocytosis or, in some cases, macropinocytosis or other endocytic routes, depending on cell context[3]. Because of this multiplicity, there is no universally acknowledged “single” receptor, and entry inhibition remains challenging as a therapeutic strategy.

Other names

DENV-2 entry receptorDengue virus serotype 2 entry receptorsDENV-2 cellular entry factorsDengue entry attachment factors

Entry inhibitors block viral attachment or fusion by interfering with viral binding to cellular entry receptors or co-receptors (e.g., via competitive inhibition, masking, or receptor downregulation)[2][3].