Why some patients of anemia are resistant to malaria?

Malaria is a recurring illness caused by a parasite Plasmodium falciparum and is transmitted by mosquito bite. It is prevalent in Africa and Asia and is a cause of over a million deaths in a year. The parasites infect the red blood cells (RBCs) but some people are found to be naturally resistant to malarial infections. Scientists were amazed of their natural resistance. Now a team of researchers have found the secret mechanism behind that resistance.

This study has been conducted by Marek Cyrklaff, of Heidelberg University in Germany, and collaborators in Germany and Burkina Faso and is published online in the November 10th issue of the journal Science.

It was known to scientists for a long time that the RBCs of some mutated gene carriers have an altered hemoglobin i.e. hemoglobin-S, which results in the hemoglobin aggregating within the cell leading to sickle cell anemia. Another type of mutation results in hemoglobin-C that results in hemolytic anemia when two copies of mutated hemoglobin are present. Both of these mutations give resistance to malaria. Scientists have found that these mutated forms of hemoglobin prevent the malaria parasite from forcible seizure of the actin filaments that give support to the cell.

With the help of powerful cryoelectron tomography, scientists have found that actin protein was in long filaments, which the parasite used to build an intracellular bridge for transport of its own protein, adhesion, to the cell, causing the cells to stick together and with the walls of the blood vessels resulting in inflammation leading to characteristic malarial responses. However, in the cells containing hemoglobin S and C this bridge for transport of proteins could not be established.

Malarial parasite establishing a bridge (yellow) with the cell
Malarial parasite establishing a bridge (yellow) with the cell
Malarial parasite is unable to establish a connection with altered hemoglobin variants
Malarial parasite is unable to establish a connection with altered hemoglobin variants

Researchers have also found that the mutated forms of hemoglobin are more easily oxidizable than the unmutated forms and when the actin filaments are placed with them, they resulted in shorter filaments than normal.

Reference:

Marek Cyrklaff, Cecilia P. Sanchez, Nicole Kilian, Cyrille Bisseye, Jacques Simpore, Friedrich Frischknecht, Michael Lanzer, (2011). Hemoglobins S and C Interfere with Actin Remodeling in Plasmodium falciparum–Infected Erythrocytes. Science, DOI: 10.1126/science.1213775

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