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Are Iron‐Scavenging Parasites Protective against Malaria?
Author(s) -
María Gloria Dominguez-Bello,
Martin J. Blaser
Publication year - 2005
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/426946
Subject(s) - malaria , scavenging , biology , microbiology and biotechnology , virology , immunology , biochemistry , antioxidant
To the Editor—Nyakeriga et al. [1] showed that, in Kenyan children, anemia was associated with a reduction in the incidence of clinical malaria. We provide a hypothesis that is based on this finding. Malaria has been a strong selector of human genes, since inherited conditions such as sickle-cell trait, thalassemias, and glucose-6-phosphate dehydrogenase deficiency provide partial protection against malaria. Because erythrocytes are central to the life cycle of Plasmodium falciparum, chronic anemia may lower host susceptibility to infection. A protective effect of iron deficiency against malaria has been supported by studies of animals [2] and humans [1]. Iron-supplementation treatment of anemia increases the risk of P. vivax malaria [3–5]. In contrast, anemia-inducing parasites, including particular helminths and nematodes [4–6], appear to offer a benefit against malaria to humans who are infected with these organisms and who live in regions in which malaria is endemic [7]. Bacteria that induce iron-deficiency anemia in humans also might confer resistance to malaria. Helicobacter pylori, a longtime colonizer of humans [8] that has been shown to cause iron-deficiency anemia [9–12], commonly colonizes human populations in tropical areas. One biological cost of infection with H. pylori, in exchange for a possible benefit in protection against malaria, might be a higher risk of peptic ulcer disease. Just as malaria may have shaped host responses to H. pylori [13], H. pylori may affect the severity of malaria in infected populations through its role in iron homeostasis. Maria G. Dominguez-Bello and Martin J. Blaser Department of Biology, University of Puerto Rico, San Juan, Puerto Rico; Departments of Medicine and Microbiology, New York University School of Medicine, New York

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