Originally, it was believed that all pathogens involved some sort of nucleic acid, whether it was DNA in bacteria or parasites or RNA in viruses. Therefore, when the symptoms of transmissible spongiform encephalopathies (TSEs) were first encountered, it was assumed that an agent containing nucleic acid caused them. The idea that a protein alone could be a disease agent was completely out of the picture. In 1972, Stanley Prusiner, a resident in the Department of Neurology at the University of California San Francisco, had a patient die from a TSE and was curious about its mechanism of infection. In 1974 he began to formally work on scrapie, a TSE present in sheep. The consensus at that time was that a slowly acting virus was responsible for TSEs, but Prusiner could not find a nucleic acid that would be responsible, only protein. In 1982, he was confident enough in his data that pointed to a protein as the responsible agent in TSEs to publish it. His data also showed that the disease-causing material resisted mechanisms that were known to break down nucleic acids, but was rendered harmless by methods that attacked proteins only. This idea was met with great skepticism as it changed the understanding of disease-causing mechanisms, but the bulk of the data supports this hypothesis. Although some scientists remain skeptical that TSEs are solely the result of infectious proteins, the majority of scientists and much of the data support the prion hypothesis. In 1997, Prusiner received the Nobel Prize in Physiology or Medicine for his work in discovering the prion mechanism of disease, which reflected an acceptance of his work and data by the scientific community (Prusiner, 1997).