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Dengue virus serotype 2 (DENV-2) prM/E envelope antigens consist of the precursor membrane (prM) and envelope (E) structural proteins, which are the primary targets for the host's neutralizing antibody response. The E protein is a type II fusion protein organized into three domains (EDI, EDII, and EDIII); it mediates viral attachment to host cell receptors and subsequent membrane fusion within the endosome. The prM protein serves as a molecular chaperone for the E protein, ensuring its proper folding and preventing premature fusion during the virus's transit through the acidic secretory pathway of the host cell. These antigens are the central components of licensed and candidate dengue vaccines, such as Dengvaxia and Qdenga, which aim to elicit protective immunity. However, a significant therapeutic challenge is antibody-dependent enhancement (ADE), where sub-neutralizing or cross-reactive antibodies (particularly those targeting prM or conserved E epitopes) facilitate viral entry into Fc-receptor-bearing cells, potentially leading to severe disease manifestations like dengue hemorrhagic fever.
Induction of neutralizing antibodies and T-cell responses (vaccines); blocking of host cell receptor binding or inhibition of pH-dependent membrane fusion (antibodies and small molecules).
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