Abstract
Severe malaria is caused by the Apicomplexan parasite Plasmodium falciparum, and results in significant global morbidity and mortality, particularly among young children and pregnant women. P. falciparum exclusively infects human erythrocytes during clinical illness, and several natural erythrocyte polymorphisms are protective against severe malaria. Since erythrocytes are enucleated and lack DNA, genetic approaches to understand erythrocyte determinants of malaria infection have historically been limited. This review highlights recent advances in the use of hematopoietic stem cells to facilitate genetic screening for malaria host factors. While challenges still exist, this approach holds promise for gaining new insights into host-pathogen interactions in malaria.
Copyright © 2017 Elsevier Ltd. All rights reserved.
MeSH terms
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CD55 Antigens / genetics*
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CD55 Antigens / immunology
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Cell Differentiation
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Child
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Disease Resistance / genetics*
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Erythrocytes / immunology
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Erythrocytes / metabolism
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Erythrocytes / parasitology
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Female
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Gene Expression
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Genome-Wide Association Study
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Hematopoietic Stem Cells / immunology
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Hematopoietic Stem Cells / metabolism
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Hematopoietic Stem Cells / parasitology
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Host-Pathogen Interactions / immunology*
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Humans
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Hyaluronan Receptors / genetics*
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Hyaluronan Receptors / immunology
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Immunity, Innate
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Malaria, Falciparum / genetics*
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Malaria, Falciparum / immunology
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Malaria, Falciparum / parasitology
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Plasmodium falciparum / immunology
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Plasmodium falciparum / metabolism*
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Plasmodium falciparum / pathogenicity
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Pregnancy
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Primary Cell Culture
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Severity of Illness Index
Substances
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CD44 protein, human
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CD55 Antigens
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Hyaluronan Receptors