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Sickle hemoglobin instability: a mechanism for malarial protection

Robert P Hebbel1

  • 1Division of Hematology-Oncology and Transplantation, Department of Medicine, and Vascular Biology Center, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA. hebbe001@tc.umn.edu

Redox Report : Communications in Free Radical Research
|February 14, 2004
PubMed

Heterozygosity for the mutant sickle hemoglobin confers protection from severe Plasmodium falciparum malaria. It is here proposed that this protection derives from the instability of sickle hemoglobin, which clusters red cell membrane protein band 3 and triggers accelerated removal by phagocytic cells. This explanation requires that sickle trait cells manifest greater hemoglobin instability than normal red cells, something that could derive from their content of sickle hemoglobin. The mechanism also implicates splenic function as a determinant of the protective effect.

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