Human adaptive immune receptors recognizing Dengue virus serotype 3 pre-membrane and envelope proteins (DENV3-prM/E receptors)

Human adaptive immune receptors recognizing Dengue virus serotype 3 (DENV-3) pre-membrane (prM) and envelope (E) proteins include B-cell receptors (antibodies) and T-cell receptors that mediate the host defense against infection (Screaton et al., 2015, PubMed: 25908815). The E protein is the primary target for neutralizing antibodies, which bind to specific epitopes such as the E-dimer epitope (EDE) or domain-specific sites (EDI, EDII, EDIII) to prevent viral attachment and fusion with host cell membranes (Fibriansah et al., 2015, PubMed: 26113643). While potent neutralizing antibodies like 5J7 are serotype-specific for DENV-3, others may be cross-reactive across the four Dengue serotypes (Pierson & Diamond, 2020, PubMed: 32814858). A significant challenge in the activity of these receptors is antibody-dependent enhancement (ADE), where sub-neutralizing concentrations of antibodies facilitate viral entry into Fc-gamma receptor-bearing cells, potentially leading to severe Dengue Hemorrhagic Fever (Katzelnick et al., 2017, PubMed: 29097548). Vaccines such as CYD-TDV and TAK-003 are designed to elicit these adaptive receptors to provide long-term immunity, though their efficacy varies by serotype and prior exposure status (Wilder-Smith, 2020, PubMed: 31980634). Understanding the structural basis of how these receptors interact with DENV-3 prM/E epitopes is crucial for developing safe, next-generation therapeutics and universal vaccines.

Other names

Anti-DENV3 antibodiesDENV3-specific T-cell receptorsDENV3 prM/E-specific BCRsDENV3-specific TCRsDENV3-neutralizing antibodiesDENV3 prM/E-specific antibodies

Neutralization of viral particles by blocking attachment or fusion; induction of cellular immunity against infected cells; potential for antibody-dependent enhancement.