A team of scientists reports that 'mad cow'-like diseases have not been a major force in human history, nor have been cannibalistic rituals that are known to be associated with disease transmission.//
In a new study published by the journal Genome Research, Prof. Jaume Bertranpetit at the Universitat Pompeu Fabra and his colleagues used a fresh set of genetic data to show that balancing selection associated with cannibalism has not been a major selective driving force on the prion protein gene, as has been recently proposed.
The study also has important implications for researchers using a specific class of DNA markers called SNPs (single nucleotide polymorphisms) for examining genetic associations with diseases or for evaluation of historical patterns of human migration.
The prion protein gene (PRNP) encodes a protein that can abnormally fold and amass in brain tissues to cause fatal neurodegenerative diseases such as mad cow disease. These diseases, cumulatively known as transmissible spongiform encephalopathies (TSEs), include CJD (Creutzfeldt-Jakob disease) and kuru in humans. Kuru is confined to a human population in Papua-New Guinea and is transmitted by cannibalism at ritualistic mortuary feasts.
A high-profile study published nearly three years ago suggested that individuals who were heterozygous for a common polymorphism in the PRNP gene were relatively resistant to the disease. Over time, homozygotes who participated in the cannibalistic rituals purportedly decreased in number due to their increased susceptibility to kuru. This indicated that cannibalism conferred an effect of balancing selection on the PRNP gene throughout human history.
Bertranpetit and his colleagues sequenced 2,378 base pairs of the PRNP gene in 174 individuals; in addition, they genotyped two SNPs from the PRNP gene in 1000 individuals from populations worldwide. They identified 28 different haplotypes - or combinations of DNA varPage: 1 2 Related medicine news :1
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