Red blood cell defects and malaria

Mol Biochem Parasitol. 2006 Oct;149(2):121-7. doi: 10.1016/j.molbiopara.2006.05.007. Epub 2006 Jun 9.

Abstract

Malaria is a major cause of childhood death throughout much of the tropical world. As a result, it has exerted a powerful force for the evolutionary selection of genes that confer a survival advantage. Identifying which genes are involved, and how they affect malaria risk, is a potentially useful way of exploring the host-parasite relationship. To date, some of the best-described malaria-protective polymorphisms relate to genes that affect the structure or function of red blood cells (RBC). Recent years have seen significant advances in our understanding of the importance of some of these genes, including glycophorin C (GYPC); complement receptor 1 (CR1); band 3 (SLC4A1); pyruvate kinase (Pklr); and the genes for alpha-(HBA) and beta-globin (HBB). The challenge for the future must be to convert these advances into fresh approaches to the prevention and treatment of malaria.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Elliptocytosis, Hereditary / blood
  • Elliptocytosis, Hereditary / parasitology
  • Erythrocytes / parasitology
  • Erythrocytes / physiology
  • Erythrocytes, Abnormal / parasitology
  • Erythrocytes, Abnormal / pathology
  • Hemoglobinopathies / blood
  • Hemoglobinopathies / parasitology
  • Host-Parasite Interactions
  • Humans
  • Malaria / blood*
  • Malaria / genetics
  • Malaria / parasitology
  • Malaria / prevention & control
  • Plasmodium / pathogenicity
  • Polymorphism, Genetic
  • Receptors, Complement 3b / blood
  • Receptors, Complement 3b / genetics
  • Thalassemia / blood
  • Thalassemia / parasitology

Substances

  • Receptors, Complement 3b