Intercellular adhesion molecule-1 is an endothelial cell adhesion receptor for Plasmodium falciparum

Article Abstract:

Malaria is a disease caused by the parasite Plasmodium falciparum, which causes red blood cells to burst, resulting in severe anemia. In the absence of treatment, death can occur, usually due to the blockage of blood vessels in the heart and in the brain by infected red blood cells. The infected red blood cells become bound to blood vessels and are thus removed from circulation. If left in circulation they would pass through the spleen and be destroyed. Researchers have been trying to identify the molecules on the infected red cells and on the blood vessels that are involved in this binding process which leads to blockage of the blood vessels. The molecules on the infected red blood cells which cause binding have not been identified. Two host molecules have been previously identified which bind infected red blood cells; thrombospondin, a protein produced by platelets, cell fragments involved in blood clotting; and CD36, a protein on the surface of endothelial cells, which line blood vessels. Another molecule present on endothelial cells that binds infected red cells has been identified, known as intercellular adhesion molecule-1 (ICAM-1). A section of DNA containing the genetic code for the production of the ICAM-1 molecule was put into cells, which can express the molecule on the cell surface. The cells that contain ICAM-1 were able to bind infected red cells. The level of ICAM-1 in cells was increased in response to various stimulations of the immune system. Increased numbers of infected red blood cells bind to the cells treated with these factors. CD36 and ICAM-1 bind red blood cells infected with some strains of P. falciparum but not others. Therefore, the parasites may use more than one molecule to bind to blood vessels in order to escape destruction in the spleen.

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Malaria: binding of infected red cells

Article Abstract:

Malaria is a disease caused by the parasite Plasmodium falciparum, which causes the red blood cells to burst, resulting in severe anemia. If treatment is not provided, death can occur, usually from blockage of blood vessels in the heart and in the brain by infected red blood cells. The infected red cells become bound to blood vessels and thus removed from circulation, where otherwise they would pass through the spleen and be destroyed. Researchers have been trying to identify the molecules on the infected red cells and on the blood vessels that are involved in this binding process. The molecules on the infected red blood cells which cause binding have not been identified, but three molecules of the host are known to bind infected red blood cells: thrombospondin, a protein produced by platelets (cells involved in blood clotting); CD36, a protein on the surface of endothelial cells, which line the blood vessels; and a recently identified molecule, ICAM-1 (intercellular adhesion molecule-1). Different strains of P. falciparum bind to different molecules, suggesting that there are different mechanisms of binding among different parasites. These different mechanisms may exist so that the parasite has alternative binding pathways to avoid destruction in the spleen and to avoid blockage of binding by the immune response of an individual against these molecules.

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Natural selection of hemi- and heterozygotes for G6PD deficiency in Africa by resistance to severe malaria

Article Abstract:

Glucose-6-phosphate dehydrogenase deficiency A-(G6PD A-), common in Africa, is found to be related to a 46%-58% risk-reduction of severe malaria for female heterozygotes and male hemiozygotes in two case-control studies of 2,000 African children. A mathematical model measuring the benefits of G6PD A- as protection from severe malaria establishes that it should take only 2,000 to 3,000 years to eradicate malaria since both males and females with G6PD A- are protected and so would be selected by evolution. The current rate of G6PD A-, 50%, would indicate a counterbalancing evolutionary disadvantage that prevented malaria eradication.

Health aspects, Prevention, Genetic aspects, Dehydrogenases, Oxidoreductases, Natural immunity, Deficiency diseases

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