Dengue virus type 2 envelope glycoprotein host cell surface receptors (DENV-2 E receptors)

The Dengue virus type 2 (DENV-2) envelope (E) glycoprotein is the primary mediator of viral entry, interacting with various host cell surface receptors to initiate infection. These receptors include C-type lectins such as DC-SIGN (CD209) on dendritic cells, L-SIGN (CLEC4M) on endothelial cells, and the mannose receptor (CD206) on macrophages, which recognize the glycans on the E protein, as well as heparan sulfate proteoglycans that act as initial attachment factors (Cruz-Oliveira et al., 2013; PMID: 23515834). Upon binding, the virus is internalized via receptor-mediated endocytosis, a process critical for the viral life cycle and the pathogenesis of Dengue fever and severe Dengue Hemorrhagic Fever (Perera-Lecoin et al., 2013; PMID: 24152977). Therapeutic strategies targeting these interactions involve the use of entry inhibitors, such as monoclonal antibodies (e.g., VIS513) that bind the E protein or small molecules that mimic host glycans to competitively inhibit viral attachment (Hidari & Suzuki, 2011; PMID: 22500133). However, a significant challenge in targeting these host receptors is their involvement in essential biological processes, including immune surveillance and cell-cell adhesion, which can lead to off-target effects. Additionally, in the case of antibody-based therapies, there is a risk of antibody-dependent enhancement (ADE), where sub-neutralizing levels of antibodies facilitate viral entry into Fc-receptor-bearing cells.

Other names

DENV-2 entry receptorsDENV-2 attachment factorsHost cell receptors for DENV-2 E proteinDengue virus serotype 2 entry receptors

Inhibition of viral attachment and entry by blocking the interaction between the viral envelope glycoprotein and host cell surface receptors.