Malaria is a tropical disease of parasitic origin transmitted by the Anopheles mosquito, caused by the protozoan of the genus Plasmodium. Around miles of people worldwide affected by disease, have been related the endemic development of genetic alterations, called erythrocyte polymorphisms. These erythrocyte polymorphisms have become tools for resistance against malaria, where they have had an impact on the appearance of hemoglobinopathies, enzymatic alterations in erythrocytes, and

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... s in the structure of erythrocytes related to membrane proteins. These sections address a detailed approach to the resistance mechanisms involved against the development of P. falciparum and develop a complete development of the principles of molecular principles that attempt to explain the functioning of these biochemical mechanisms and the development of the parasite. Plasmodium falciparum Protein Exported in Erythrocyte and Mechanism Resistance to Malaria DOI: http://dx.doi.org/10.5772/intechopen.83700 the red blood cells and initiate the intra-erythrocyte stage, which lasts approximately 48 hours. Immediately after the invasion, the growth and development staging begins first as rings (0-24 h), then as trophozoites (24-40 h), and finally as schizonts (40-48 h); the cycle ends with the host cell destruction and the release of new merozoites from circulating erythrocytes, then initiating another cycle [6] (Figure 1) . During the development and growth stages, the parasite causes successive changes in the architecture of the infected erythrocyte (remodeling), which are fundamental for its vital functions. These changes are the acquisition of extracellular environment nutrients, the attribution of cytoadhesive properties that contribute to spleen-clearance evasion, the generation of changes in the host membrane cytoskeleton that are necessary for efficient parasite progeny release, and the formation of new organelles, such as the Maurer's clefts, tubulovesicular network, and the parasitophorous vacuole membrane (PVM) (Figure 2) [7, 8] . When the parasite enters the erythrocyte, it locates inside a parasitophorous vacuole (PV), which isolates it from the host cell cytoplasm, through the PVM. From then on, pathogen survival will depend on the efficient traffic of the molecules through the PVM and the plasma membrane [4, 9] .