Abstract |
The historical association between Plasmodium and primates has meant that many Plasmodium species have coevolved with specific primate hosts. However, unlike humans that are infected by species such as P. falciparum that cause severe malaria, many non-human primates are infected by Plasmodium species that only cause mild disease. Here we investigate whether the genomic signatures of plasmodial infection found in humans are also present in chimpanzees. We find no evidence of the major deleterious mutations at HBB ( beta-globin) and G6PD in chimpanzees that confer resistance to malaria caused by P. falciparum nor evidence of long-term balancing selection at these loci. Our knowledge of malaria prevalence and pathogenesis in wild chimpanzees is severely limited, but it may be the case that beta-globin and G6PD variation are not adaptive in chimpanzees because malaria is rare and/or less detrimental in this species. Alternatively, chimpanzees may utilise mechanisms that are different from those of humans to protect against malaria.
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Authors | T S MacFie, E Nerrienet, R E Bontrop, N I Mundy |
Journal | Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases
(Infect Genet Evol)
Vol. 9
Issue 6
Pg. 1248-52
(Dec 2009)
ISSN: 1567-7257 [Electronic] Netherlands |
PMID | 19631293
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- beta-Globins
- Glucosephosphate Dehydrogenase
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Topics |
- Animals
- Evolution, Molecular
- Genetic Variation
- Genome
- Glucosephosphate Dehydrogenase
(genetics)
- Host-Parasite Interactions
(genetics)
- Humans
- Immunity, Innate
(genetics)
- Malaria, Falciparum
(immunology, parasitology, physiopathology)
- Pan troglodytes
- Plasmodium falciparum
(pathogenicity, physiology)
- Selection, Genetic
- Species Specificity
- Virulence
- beta-Globins
(genetics)
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