February 24, 2006 | Alan F. Cowman1,* and Brendan S. Crabb1,*
The malaria parasite, a member of the Apicomplexa phylum, is a significant cause of morbidity and mortality worldwide. The invasion of host cells by these parasites is a critical step in their life cycle, allowing them access to nutrients and protection from host defenses. All Apicomplexa share a common mode of host-cell entry, but individual species have unique features and ligand-receptor interactions. The malaria parasite, *Plasmodium*, primarily invades erythrocytes, with *P. falciparum* being the most severe form of malaria. The invasion process involves several key steps, including initial recognition and attachment, followed by the formation of a tight junction powered by the parasite's actin-myosin motor. The surface proteins of the merozoite, such as AMA-1 and MSP-1, play crucial roles in these processes. The invasion machinery is highly conserved across Apicomplexan parasites, suggesting a common evolutionary origin. However, the specific ligands and receptors used by different species vary, providing a mechanism for phenotypic variation and resistance to immune responses. Understanding the detailed mechanisms of malaria parasite invasion is essential for developing new treatments and vaccines.The malaria parasite, a member of the Apicomplexa phylum, is a significant cause of morbidity and mortality worldwide. The invasion of host cells by these parasites is a critical step in their life cycle, allowing them access to nutrients and protection from host defenses. All Apicomplexa share a common mode of host-cell entry, but individual species have unique features and ligand-receptor interactions. The malaria parasite, *Plasmodium*, primarily invades erythrocytes, with *P. falciparum* being the most severe form of malaria. The invasion process involves several key steps, including initial recognition and attachment, followed by the formation of a tight junction powered by the parasite's actin-myosin motor. The surface proteins of the merozoite, such as AMA-1 and MSP-1, play crucial roles in these processes. The invasion machinery is highly conserved across Apicomplexan parasites, suggesting a common evolutionary origin. However, the specific ligands and receptors used by different species vary, providing a mechanism for phenotypic variation and resistance to immune responses. Understanding the detailed mechanisms of malaria parasite invasion is essential for developing new treatments and vaccines.