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G6PD Deficiency Is Associated With Significant Protection Against Severe, Life-threatening Malaria

Date:
March 13, 2007
Source:
Public Library of Science
Summary:
A case-control study in two populations in Mali, West Africa has shown that glucose-6-phosphate dehydrogenase (G6PD) deficiency is associated with significant protection against severe, life-threatening malaria.

G6PD (A-) deficiency, an X chromosome trait prevalent in Africa, protected hemizygous male children but not heterozygous female children against progression of malaria into life-threatening complications.
Credit: Thomas Wellems; Public Library of Science

A case-control study in two populations in Mali, West Africa has shown that glucose-6-phosphate dehydrogenase (G6PD) deficiency is associated with significant protection against severe, life-threatening malaria. Researchers from the US National Institute of Allergy and Infectious Diseases and the University of Bamako, Mali, led by Thomas E. Wellems, report the findings this week in the journal PLoS Medicine.

G6PD deficiency is also known as "favism" after the Italian word for broad beans (fava) which cause a classic reaction when eaten by people with G6PD deficiency. In males, who have only one X chromosome, mutations in the gene for G6PD on the X chromosome cause G6PD deficiency. Females who have mutations on both X chromosomes will also be deficient. G6PD is an important enzyme in red blood cells (erythrocytes), the host cells for Plasmodium falciparum, the parasite that causes the most severe form of malaria. G6PD deficiency is associated with protection against malaria, notably in Africa where one form of G6PD deficiency (G6PD A-) is widespread.

In the two populations of more than 3000 children studied in rural Mali where malaria is very frequent, G6PD deficiency in male and female children was associated with protection against severe, life-threatening malaria, but no effect was found in females who had just one abnormal gene. However, there was no significant difference in the numbers of parasites in the red blood cells of the various groups of children indicating that the deficiency does not work by stopping parasites from infecting the children.

G6PD deficiency instead appears to mitigate disease processes set up by the parasitized cells in the bloodstream. The protection was confirmed by a combined analysis of these data and data from a previous study. Protection was most evident against cerebral malaria, the most frequent form of life-threatening malaria in these studies.

These results reignite the debate about the relationship between G6PD deficiency and protection against malaria. They are particularly relevant in populations such as the one studied where, as the authors note, because "virtually all young children experience episodes of malaria, such protective hemoglobinopathies and erythrocyte polymorphisms offer a tremendous survival benefit when they prevent progression of uncomplicated malaria."

Reference: http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0040066

Citation: Guindo A, Fairhurst RM, Doumbo OK, Wellems TE, Diallo DA (2007) X-linked G6PD deficiency protects hemizygous males but not heterozygous females against severe malaria. PLoS Med 4(3): e66.


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The above story is based on materials provided by Public Library of Science. Note: Materials may be edited for content and length.


Cite This Page:

Public Library of Science. "G6PD Deficiency Is Associated With Significant Protection Against Severe, Life-threatening Malaria." ScienceDaily. ScienceDaily, 13 March 2007. <www.sciencedaily.com/releases/2007/03/070313114502.htm>.
Public Library of Science. (2007, March 13). G6PD Deficiency Is Associated With Significant Protection Against Severe, Life-threatening Malaria. ScienceDaily. Retrieved July 30, 2014 from www.sciencedaily.com/releases/2007/03/070313114502.htm
Public Library of Science. "G6PD Deficiency Is Associated With Significant Protection Against Severe, Life-threatening Malaria." ScienceDaily. www.sciencedaily.com/releases/2007/03/070313114502.htm (accessed July 30, 2014).

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