Flavivirus entry at host cell surface

Flavivirus entry at host cell surface refers to the multi-step process by which viruses such as Dengue, Zika, and West Nile infect host cells. This process is initiated by the viral Envelope (E) protein, which mediates attachment to host cell surface factors like heparan sulfate proteoglycans and specific receptors such as DC-SIGN, TIM-1, and AXL (Perera-Lecoin et al., 2013; Hamel et al., 2015). Following attachment, the virus is internalized through clathrin-mediated endocytosis (Smit et al., 2011). The acidic environment within the endosome triggers a structural rearrangement of the E protein from a dimer to a trimer, facilitating the fusion of the viral envelope with the endosomal membrane (Harrison, 2008). This fusion event releases the viral genome into the cytoplasm for replication. Therapeutic interventions targeting this process include monoclonal antibodies that neutralize the E protein and small molecules like suramin or epigallocatechin gallate that block attachment or fusion (Wang et al., 2017). A major safety concern in developing entry inhibitors is antibody-dependent enhancement (ADE), where non-neutralizing antibodies facilitate viral entry into immune cells, potentially increasing disease severity (Katzelnick et al., 2017).

Other names

Flavivirus attachmentFlavivirus internalizationFlavivirus membrane fusionViral entry

Inhibition of viral attachment to host cell receptors, prevention of E protein conformational changes required for membrane fusion, or interference with endosomal acidification.