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Joan Stephenson, PhD

JAMA. 2001;285:2847.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

The discovery by British researchers that genes other than the prion protein gene may play a role in the development of the human form of bovine spongiform encephalopathy (BSE) is prompting speculation that the disease may have a longer incubation period in some people. If this proves to be the case, estimates made last year based on the assumption that only 40% of the British population were at risk of developing the variant form of Creutzfeldt-Jakob disease (vCJD) would have be revised upward.

The new findings were published in the May 22 issue of Proceedings of the National Academy of Sciences.

Studies with infected inbred strains of mice have found large differences in the time between infection and onset of symptoms of the brain disorder, even when the animals have prion protein with identical amino acid sequences—suggesting that additional genes may play a role. In the . . . [Full Text of this Article]

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