Nature's Way of Protection: Innate Resistance to Malaria
Ernst Hempelmann*
Center of Cellular and Molecular Biology of Diseases, Instituto de Investigaciones Científicas y Servicios de Alta Tecnología (INDICASAT AIP), City of Knowledge, Republic of Panama
*Corresponding Author: Ernst Hempelmann, Center of Cellular and Molecular Biology of Diseases, Instituto de Investigaciones Científicas y Servicios de Alta Tecnología (INDICASAT AIP), City of Knowledge, Republic of Panama.
Received:
May 24, 2021; Published: June 09, 2021
Abstract
The malaria parasite has co-evolved with its human host. This has had a profound effect on the genetic variability in host response to malaria.
This review will focus on RBC modifications, such as sickle cell, thalassemia’s, glucose-6-phosphate dehydrogenase deficiency and ovalocytosis frequent in persons living in endemic malaria settings.
Keywords: Malaria; Hemoglobin; Sickle Cell
References
- Aidoo M., et al. “Protective effects of the sickle cell gene against malaria morbidity and mortality”. Lancet 9314 (2002): 1311-1312.
- Alcaïs A., et al. “Human genetics of infectious diseases: between proof of principle and paradigm”. Journal of Clinical Investigation9 (2009): 2505-2514.
- Allison AC. “Notes on sickle-cell polymorphism”. Annals of Human Genetics 19 (1954a): 39-57.
- Allison AC. “The distribution of the sickle-cell trait in East Africa and elsewhere, and its apparent relationship to the incidence of subtertian malaria”. Transactions of the Royal Society of Tropical Medicine and Hygiene4 (1954b): 312-318.
- Allison AC. “Protection Afforded by Sickle-cell Trait Against Subtertian Malaria Infection”. British Medical Journal4857 (1954c): 290-294.
- Allison AC. “Aspects of polymorphism in man”. Cold Spring Harbor Symposia on Quantitative Biology 20 (1955): 239-251.
- Allison AC and Clyde DF. “Malaria in African Children with Deficient Erythrocyte Glucose-6-phosphate Dehydrogenase”. British Medical Journal5236 (1961): 1346-1349.
- Allison AC. “The discovery of resistance to malaria of sickle-cell heterozygotes”. Biochemistry and Molecular Biology Education 30 (2002): 279-287.
- Allison AC. “Genetic control of resistance to human malaria”. Current Opinion in Immunology5 (2009a): 499-505.
- Allison AC. “A sickle-cell safari, chapter 8”. in: Sean B Carroll Into the Jungle: Great adventures in the search for evolution, San Francisco, Pearson Benjamin Cummings (2009b): 148-165.
- Alving AS., et al. “Enzymatic deficiency in primaquine-sensitive erythrocytes”. Science 3220 (1956): 484-485.
- Anstey NM., et al. “Lung Injury in Vivax Malaria: Pathophysiological Evidence for Pulmonary Vascular Sequestration and Posttreatment Alveolar-Capillary Inflammation”. Journal of Infectious Diseases 4 (2007): 589-596.
- Barnwell JW., et al. “In vitro evaluation of the role of the Duffy blood group in erythrocyte invasion by Plasmodium vivax”. Journal of Experimental Medicine 5 (1989): 1795-1802.
- Beutler E. “Glucose-6-phosphate dehydrogenase deficiency: a historical perspective”. Blood 1 (2008): 16-24.
- Brain P. “Sickle-cell Anaemia in Africa”. British Medical Journal 2 (1952): 880.
- Canali S. “Researches on thalassemia and malaria in Italy and the origins of the "Haldane hypothesis". Medicina nei Secoli 3 (2008): 827-846.
- Cavasini CE., et al. “Duffy the Brazilian Amazon region”. Malaria Journal1 (2007): 167.
- Ceppellini R. “Discussion of "Aspects of Polymorphism in Man”. Cold Spring Harbor Symposia on Quantitative Biology 20 (1955): 251-255.
- Culleton RL., et al. “Failure to detect Plasmodium vivax in West and Central Africa by PCR species typing”. Malaria Journal1 (2008): 174.
- Flatz G. “Hemoglobin E: distribution and population dynamics”. Humangenetik 3 (1967): 189-234.
- Flint J., et al. “The population gentics of the haemoglobinopathies”. Balliere’s Clinical Haematology 6 (1993): 215-262.
- Guindo A., et al. “X-linked G6PD deficiency protects hemizygous males but not heterozygous females against severe malaria”. PLoS Medicine3 (2007): e66.
- Hahn EV and Gillespie EB. "Sickle cell anemia. Report of a case greatly improved by splenectomy. Experimental study of sickle cell formation”. Archives of Internal Medicine 2 (1927): 233-254.
- Herrick JB. “Peculiar elongated and sickle-shaped red blood corpuscles in a case of severe anemia”. Archives of Internal Medicine 5 (1910): 517-521. Reprinted in Herrick JB (2001) Peculiar elongated and sickle-shaped red blood corpuscules in a case of severe anemis 1910. Yale J Biol Med 74.3 (1910): 179-184.
- Hutagalung R., et al. “Influence of hemoglobin E trait on the severity of Falciparum malaria”. Journal of Infectious Diseases 1 (1999): 283-286.
- Ingram VM. “Abnormal human haemoglobins. III. The chemical difference between normal and sickle cell haemoglobins”. Biochimica et Biophysica Acta 2 (1959a): 402-411.
- Ingram VM and Stretton AO. “Genetic basis of the thalassaemia diseases”. Nature 4703 (1959b): 1903-1909.
- Jarolim P., et al. “Deletion in erythrocyte band 3 gene in malaria-resistant Southeast Asian ovalocytosis”. Proceedings of the National Academy of Sciences of the United States of America 24 (1991): 11022-11026.
- Labie D., et al. “Haplotypes in tribal Indians bearing the sickle-gene: evidence for the unicentric origin of the ßS mutation and the unicentric origin of tribal populaton in India”. Human Biology4 (1989): 479-491.
- Lapouméroulie C., et al. “A novel sickle cell mutation of yet another origin in Africa: the Cameroon type”. Human Genetics 3 (1992): 333-337.
- Lebby R. “Case of absence of the spleen”. Southern Medical Journal 1 (1846): 481-483.
- Lehmann H and Raper AB. “Distribution of sickle cell trait in Uganda, and its ethnological significance”. Nature 4168 (1949): 494-495.
- Lehmann H and Cutbush M. “Sickle cell trait in southern India”. British Medical Journal 6 (1952): 404-405.
- Liu SC., et al. “Molecular defect of the band 3 protein in southeast Asian ovalocytosis”. The New England Journal of Medicine 22 (1990): 1530-1538.
- López C., et al. “Mechanisms of genetically-based resistance to malaria”. Gene 1-2 (2010): 1-12.
- Luzzatto L., et al. “Glucose-6-phosphate dehydrogenase deficient red cells: Resistance of infection by malaria parasites”. Science 164 (1969): 839-841.
- Mason VR. “Sickle cell anemia”. JAMA 79 (1922): 1318-1320.
- May J., et al. “Hemoglobin variants and disease manifestations in severe falciparum malaria”. JAMA 20 (2007): 2220-2226.
- Ménard D., et al. “Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people”. Proceedings of the National Academy of Sciences of the United States of America13 (2010): 5967-5971.
- Mendes C., et al. “Duffy negative antigen is no longer a barrier to Plasmodium vivax - molecular evidences from the African West Coast (Angola and Equatorial Guinea)”. PLOS Neglected Tropical Diseases 6 (2011): e1192.
- Miller LH., et al. “The resistance factor to Plasmodium vivax in blacks. The Duffy-blood-group genotype, FyFy”. The New England Journal of Medicine6 (1976): 302-304.
- Modiano G., et al. “Protection against malaria morbidity: near-fixation of alpha-thalassemia gene in a Nepalese population”. American Journal of Human Genetics 48 (1991): 390-397.
- Modiano D., et al. “Haemoglobin C protects against clinical Plasmodium faciparum malaria”. Nature 6861 (2001): 305-308.
- Montalenti G. “Comment on Haldane, JBS. Disease and evolution”. Rice Science 19 (1949): 333-334.
- Pauling L., et al. “Sickle cell anemia, a molecular disease”. Science2865 (1949): 543-548.
- Piel FB., et al. “Global distribution of the sickle gene and geographical confirmation of the malaria hypothesis”. Nature Communication8 (2010): 1-7.
- Ryan JR., et al. “Evidence for transmission of Plasmodium vivax among a duffy antigen negative population in Western Kenia”. American Society of Tropical Medicine and Hygiene 4 (2006): 575-581.
- Santos-Ciminera PD., et al. “Malaria Diagnosis and Hospitalization Trends, Brazil”. Emerging Infectious Diseases 10 (2007): 1597-1600.
- Stamatoyannopoulos G and Fessas P. “Thalassemia, glucose-6-phosphate dehydrogenase deficiency, sickling and malarial endemicity in Greece. A study of five areas”. British Medical Journal5387 (1964): 875-879.
- Terrenato L., et al. “Decreased malaria morbidity in the Tharu people compared to sympatric populations in Nepal”. Annals of Tropical Medicine and Parasitology 1 (1988): 1-11.
- Tournamille C., et al. “Disruption of a GATA motif in the Duffy gene promotor abolishes erythroid gene expression in Duffy-negative individuals”. Nature Genetics2 (1995) 224-228.
- Wertheimer SP and Barnwell JW. “Plasmodium vivax interaction with the human Duffy blood group glycoprotein: identification of a parasite receptor-like protein”. Experimental Parasitology 4 (1989): 340-350.
- World Malaria Report 2014, World Health Organization, 20 Avenue Appia, CH-1211 Geneva 27, Switzerland (2014).
- Williams TN., et al. “Negative epistasis between the malaria-protective effects of alpha+-thalassemia and the sickle cell trait”. Nature Genetics 37 (2005): 1253-1257.
Citation
Copyright