Plasmodium falciparum infected red cells

Lauer, S. A. Chatterjee, S. Haidar, K. Uptake and hydrolysis of sphingomyelin analogues in Plasmodium falciparum-infected red cells. Mol. Biochem. Parasitol. 2001, 115, 275-281. 

Rock, E. P., Roth, E. F., Jr., Rojas-Corona, R. R., Sherwood, J. A., Nagel, R. L., Howard, R. J., and Kaul, D. K. (1988). Thrombospondin mediates the cytoadherence of Plasmodium falciparum-infected red cells to vascular endothelium in shear flow conditions. Blood 71, 71-75. 

Chakravorty, S. J., Carret, C., Nash, G. B., Ivens, A., Szestak, T., and Craig, A. G. (2007). Altered phenotype and gene transcription in endothelial cells, induced by Plasmodium falciparum-infected red blood cells Pathogenic or protective Int. J. Parasitol. 37,975-987. 

Cooke, B. M., Lingelbach, K., Bannister, L. H., and Tilley, L. (2004a). Protein trafficking in Plasmodium falciparum-infected red blood cells. Trends Parasitol. 20,581-589. 

Ginsburg, H., Kutner, S., Krugliak, M., and Cabantchik, Z. I. (1985). Characterization of permeation pathways appearing in the host membrane of Plasmodium falciparum infected red blood cells. Mol. Biochem. Parasitol. 14, 313-322. 

Luersen, K., Walter, R. D., and Muller, S. (2000). Plasmodium falciparum-infected red blood cells depend on a functional glutathione de novo synthesis attributable to an enhanced loss of glutathione. Biochem. ]. 346(Pt 2), 545-552. 

Grellier, P., Rigomier, D., Clavey, V., Fruchart, J.-C. and Schrevel, J. (1991) Lipid traffic between high density lipoproteins and Plasmodium falciparum-infected red blood cells. J. Cell Biol. 112 261-111. 

Adovelande J, Boulard Y, Berry J-P, Galle P, Slodzian G, Schrevel J. Detection and cartography of the fluorinated antimalarial drug mefloquine in normal and Plasmodium falciparum infected red blood cells by scanning ion microscopy and mass spectrometry. Biol Cell 1994 81 185-192. 

Most of the work on membrane transport with malaria parasites prior to 1990 concerned itself with studies of bird, murine and monkey plasmodia (Plasmodium lophurae, P. berghei and P. knowlesi) and this was summarized some 20 years ago (Sherman, 1979,1988). With the successful in vitro culture of P. falciparum, membrane-transport phenomena of malaria-infected red cells and free parasites have concerned themselves principally with this species and this too has been the subject of periodic review (e.g. see Kirk s tour de force, 2001). 

Roth, E. F., Jr., Schulman, S., Vanderberg, J., and Olson, J. (1986). Pathways for the reduction of oxidized glutathione in the Plasmodium falciparum-infected erythrocyte Can parasite enzymes replace host red cell glucose-6-phosphate dehydrogenase Blood 67,827-830. 

Staines, H. M., Ashmore, S., Felgate, H., Moore, J., Powell, T., and Ellory, J. C. (2006). Solute transport via the new permeability pathways in Plasmodium falciparum-infected human red blood cells is not consistent with a simple single-channel model. Blood 108,3187-3194. Staines, H. M., Ellory, J. C., and Kirk, K. (2001). Perturbation of the pump-leak balance for Na(+) and K(+) in malaria-infected erythrocytes. Am. J. Physiol. Cell Physiol. 280, C1576-C1587. 

Over 100 Plasmodium species contribute to the spread of malaria, but only four of these (P. falciparum, P. vivax, P. ovale, and P. malariae) account for human infection, the deadliest being P. falciparum. The malaria life cycle exists first in a mosquito, and then it passes to a human host. An infected female Anopholes mosquito is the host of the parasite s sporogonic hfe cycle. Mature P. falciparum sporozoites reach the salivary glands of the mosquito, and the parasite is transmitted to a human host when the mosquito feeds. During this blood meal, sporozoites are released into the bloodstream where they penetrate hepatic cells and mature into schizonts. The liver cells rupture after approximately two weeks, discharging merozoites into the bloodstream whereupon they infect red blood cells (RBCs). Every 48 to 78 hours, mature merozoites rupture from... 

Sickle cell gene mutation offers partial protection against serious malarial infection. Abnormal red blood cells (RBCs) are less easily parasitized by Plasmodium falciparum than normal RBCs. Consequently, persons with heterozygous sickle gene (SCT) have a selective advantage in regions (tropical areas) where malaria is endemic. The incidence of the sickle gene in a population correlates with the historical incidence of malaria. 

Waller, K. L., Nunomura, W., An, X., Cooke, B. M., Mohandas, N., and Coppel, R. L. (2003). Mature parasite-infected erythrocyte surface antigen (MESA) of Plasmodium falciparum binds to the 30-kDa domain of protein 4.1 in malaria-infected red blood cells. Blood 102, 1911-1914. 

Waterkeyn, J. G., Wickham, M. E., Davern, K. M., Cooke, B. M., Coppel, R. L., Reeder, J. C., Culvenor, J. G., Waller, R. F., and Cowman, A. F. (2000). Targeted mutagenesis of Plasmodium falciparum erythrocyte membrane protein 3 (PfEMP3) disrupts cytoadherence of malaria-infected red blood cells. EMBO ]. 19, 2813-2823. 

Winograd, E., and Sherman, I. W. (1989). Characterization of a modified red cell membrane protein expressed on erythrocytes infected with the human malaria parasite Plasmodium falciparum Possible role as a cytoadherent mediating protein. J. Cell Biol. 108, 23-30. 

The most severe form of malaria is caused by Plasmodium falciparum and can be fatal. Fever occurs every third day due to rupture of infected red blood cells. Other forms are less severe and rarely fatal. 

Probably no disease has killed more humans throughout history than malaria. Malaria is transmitted by the bite of an Anopheles mosquito. There are four different parasites that can infect humans, but Plasmodium falciparum is the most virulent. The parasite first migrates to the liver where after several replications the parasites are released into the bloodstream. The parasite then invades the red blood cells and feeds off the hemoglobin. Survival of the parasite relies on the ability of the parasite to package the toxic heme metabolites formed during hemoglobin metabolism in nontoxic hemazoin particles. The parasite causes anemia, fevers, chills, veno-occlusive disorders, liver damage, and death. 

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