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It was not by the time that the Kuru disease had spread into an epidemic when Daniel Carleton Gajdusek, a virologist, and Vincent ZIgas, a medical doctor, first started doing research on the disease in 1957. It was first noted in the Fore, Yate and Usanufa people in 1952-1953 by anthropologists Ronald Berndt and Catherine Berndt. After the disease had festered into a bigger epidemic the tribal people called to Charles Pfarr, a Lutheran Medical Officer to come to the area to report the disease to Australian authorities.

In effort to understand the pathology of Kuru disease, Gajdusek established the first experimental tests on chimpanzees for Kuru at the National Institutes of Health (NIH). The methods of the experiment would be to introduce the kuru brain material to the closest human relative, the chimpanzee, and to document the behaviors of until death or a negative outcome would occur. Michael Alpers, an Australian doctor, collaborated with Gajdusek in providing the samples of brain tissues he had taken from an 11-year-old Fore girl who had died of Kuru. In his work he was also the first to document the first bibliography of the Kuru disease. Gajdusek was joined by a man named Joe Gibbs to monitor and record the behavior of the apes and conduct autopsies. Within two years, one of the chimps, Daisy, had developed kuru, demonstrating that the unknown disease factor was transmitted through infected biomaterial and that it was capable of crossing the species barrier to other primates. After confirmation from Elisabeth Beck, this experiment brought about the first conducted transmission of Kuru and was deemed an very important finding in the advancement of human medicine leading to the award of a Nobel Prize to D. Carleton Gajdusek in 1976.

Subsequently, E. J. Field spent large parts of the late 1960s and early 1970s in New Guinea investigating the disease, connecting it to scrapie and multiple sclerosis. He noted similarities in the diseases interactions with glial cells, including the critical observation that the infectious process may depend on structural rearrangement of the host's molecules. This was an early observation of what was to later become the prion hypothesis.