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Enterovirus A71 (EV-A71) is a major human pathogen within the Picornaviridae family, recognized as a primary cause of hand, foot, and mouth disease (HFMD), particularly in children under five years of age (Source: WHO). The EV-A71 virion is an icosahedral structure composed of 60 protomers, each consisting of four structural proteins: VP1, VP2, VP3, and VP4. These proteins form the capsid shell that protects the viral RNA and facilitates entry into host cells by interacting with receptors such as Scavenger Receptor Class B Member 2 (SCARB2) and P-selectin Glycoprotein Ligand-1 (PSGL-1) (Source: UniProt P03300). The epitopes located on the surface-exposed loops of VP1, VP2, and VP3 are the critical targets for neutralizing antibodies, making them the focus of vaccine development and therapeutic antibody research (Source: PubMed PMID: 31431548). While most EV-A71 infections are self-limiting, the virus is neurotropic and can cause severe complications including encephalitis, meningitis, and cardiopulmonary failure. Current therapeutic strategies primarily involve inactivated vaccines that elicit a robust immune response against these capsid epitopes to prevent viral infection and spread (Source: PubMed PMID: 26796327).
Induction of neutralizing antibodies that bind to specific capsid epitopes (primarily on VP1, VP2, and VP3) to block viral attachment to host receptors and prevent viral uncoating (Source: PubMed PMID: 22383805).
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