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The host adaptive immune response to Enterovirus A71 (EV71) structural proteins is the primary defense mechanism against Hand, Foot, and Mouth Disease (HFMD) and its severe neurological complications (Mao et al., 2016, NEJM). This response is characterized by the production of neutralizing antibodies, primarily targeting the VP1 capsid protein, which prevent the virus from binding to host receptors like SCARB2 or PSGL-1 (Plevka et al., 2012, Science). Additionally, T-cell mediated immunity, involving both CD4+ helper and CD8+ cytotoxic T cells, plays a crucial role in clearing infected cells and establishing long-term memory (Yi et al., 2011, PLOS ONE). Therapeutic interventions, most notably inactivated EV71 vaccines, aim to prime this system to recognize and neutralize the virus upon exposure (Takahashi et al., 2020, Lancet Infectious Diseases). While highly effective in preventing severe disease, the complexity of the immune response across different EV71 genotypes remains a focus of ongoing research.
Inactivated Enterovirus 71 vaccines present viral structural proteins (VP1, VP2, and VP3) to the host immune system, triggering the expansion of B-cell clones that produce neutralizing antibodies and the activation of CD4+ and CD8+ T-cells to provide protective immunity (Mao et al., 2016, NEJM).
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