In a new study published by the journal Genome Research, 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. Prof. Jaume Bertranpetit, a scientist 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 recently been proposed. Their work also has important scientific implications for researchers using a specific class of DNA markers called SNPs (single nucleotide polymorphisms) to examine genetic associations with diseases or to evaluate 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 are cumulatively known as transmissible spongiform encephalopathies (TSEs) and in humans, include CJD (Creutzfeldt-Jakob disease) and kuru. 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 diminished in numbers 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 (or single nucleotide polymorphisms) from the PRNP gene in 1000 individuals from population
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Contact: Maria Smit
smit@cshl.edu
516-422-4013
Cold Spring Harbor Laboratory
3-Jan-2006

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