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The Zika virus envelope (E) and precursor membrane (prM) proteins are the primary structural components of the Zika virus (ZIKV) virion and serve as the major targets for the host immune response. The E protein is a class II viral fusion protein responsible for viral attachment to host cell receptors and mediating the fusion of viral and endosomal membranes during entry. The prM protein acts as a molecular chaperone for the E protein, preventing its premature fusion during viral assembly and maturation within the host cell's secretory pathway. Together, these proteins contain the critical epitopes recognized by B cell receptors (BCRs) and are the focus of therapeutic development, including neutralizing monoclonal antibodies and various vaccine platforms (DNA, mRNA, and inactivated). A significant challenge in targeting these proteins is the potential for antibody-dependent enhancement (ADE), where non-neutralizing or cross-reactive antibodies, particularly from prior Dengue virus exposure, can facilitate viral entry into immune cells and potentially exacerbate disease severity.
Neutralization of viral particles, inhibition of viral attachment to host cells, blockade of pH-dependent membrane fusion, and induction of protective humoral immunity through B cell receptor activation.
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