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Apical membrane antigen 1 (AMA1) is a highly conserved, type I integral membrane protein located in the micronemes of Plasmodium vivax and other apicomplexan parasites (Pizarro et al., 2005, PubMed: 15806113). It is essential for the invasion of host cells, facilitating the entry of merozoites into erythrocytes and sporozoites into hepatocytes (Remarque et al., 2008, PubMed: 18234169). During the invasion process, AMA1 is translocated to the parasite surface where it binds to rhoptry neck protein 2 (RON2), forming a moving junction that is critical for internalization (Srinivasan et al., 2011, PubMed: 21478870). Due to its indispensable role in the parasite life cycle, PvAMA1 is a major target for blood-stage malaria vaccines and inhibitory molecules (Arevalo-Herrera et al., 2015, PubMed: 25644337). However, the high degree of genetic polymorphism in the PvAMA1 gene leads to significant antigenic variation, which presents a major challenge for developing a vaccine that provides broad protection against diverse parasite strains (Arnott et al., 2014, PubMed: 24454710). Current therapeutic strategies focus on inducing neutralizing antibodies or using peptides to disrupt the AMA1-RON2 interaction (Vulliez-Le Normand et al., 2012, PubMed: 22566538).
Inhibition of the interaction between AMA1 and RON2 to prevent the formation of the moving junction and subsequent parasite entry into host cells (Srinivasan et al., 2011, PubMed: 21478870).
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