Toxoplasma and reaction time: role of toxoplasmosis in the origin, preservation and geographical distribution of Rh blood group polymorphism
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
18752708
DOI
10.1017/s003118200800485x
PII: S003118200800485X
Knihovny.cz E-resources
- MeSH
- Blood Donors * MeSH
- Adult MeSH
- Heterozygote MeSH
- Rh-Hr Blood-Group System analysis blood genetics MeSH
- Humans MeSH
- Evolution, Molecular MeSH
- Military Personnel MeSH
- Polymorphism, Genetic * MeSH
- Antibodies, Protozoan blood MeSH
- Psychomotor Performance MeSH
- Reaction Time * physiology MeSH
- Selection, Genetic MeSH
- Toxoplasma immunology pathogenicity MeSH
- Toxoplasmosis parasitology prevention & control MeSH
- Animals MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Rh-Hr Blood-Group System MeSH
- Antibodies, Protozoan MeSH
- Rho(D) antigen MeSH Browser
The RhD protein which is the RHD gene product and a major component of the Rh blood group system carries the strongest blood group immunogen, the D-antigen. This antigen is absent in a significant minority of the human population (RhD-negatives) due to RHD deletion or alternation. The origin and persistence of this RhD polymorphism is an old evolutionary enigma. Before the advent of modern medicine, the carriers of the rarer allele (e.g. RhD-negative women in the population of RhD-positives or RhD-positive men in the population of RhD-negatives) were at a disadvantage as some of their children (RhD-positive children born to pre-immunized RhD-negative mothers) were at a higher risk of foetal or newborn death or health impairment from haemolytic disease. Therefore, the RhD-polymorphism should be unstable, unless the disadvantage of carriers of the locally less abundant allele is counterbalanced by, for example, higher viability of the heterozygotes. Here we demonstrated for the first time that among Toxoplasma-free subjects the RhD-negative men had faster reaction times than Rh-positive subjects and showed that heterozygous men with both the RhD plus and RhD minus alleles were protected against prolongation of reaction times caused by infection with the common protozoan parasite Toxoplasma gondii. Our results suggest that the balancing selection favouring heterozygotes could explain the origin and stability of the RhD polymorphism. Moreover, an unequal prevalence of toxoplasmosis in different countries could explain pronounced differences in frequencies of RhD-negative phenotype in geographically distinct populations.
References provided by Crossref.org
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