PRION DISEASES OF HUMANS AND ANIMALS: Their Causes and Molecular Basis

Their Causes and Molecular Basis

2001 Annual Review of Neuroscience 24:519-50 by John Collinge


Predictions of Epidemic Size
BSE can be readily transmitted to mice with most, if not all, inoculated animals succumbing to disease on primary passage (a high "attack rate"). This relatively modest species barrier has been formally measured by comparative titration studies of the same BSE isolate by intracerebral inoculation into cattle and mice. It indicates an approximately 1000-fold barrier (i.e. it takes 1000 times more BSE to kill a mouse than a cow) (Wells et al 1998). The effect of this barrier on incubation periods is to increase mean incubation periods by approximately threefold and to dramatically increase the range of incubation periods seen.

Such experiments are usually performed using the most efficient, intracerebral, route of transmission. A formal titration of BSE in mice to determine an oral LD 50 has not been reported. [LD50 means the dose at which 50% of the subjects die--BSE coordinator] However, oral challenge with approximately 10 g of BSE-affected cow brain killed the majority of exposed mice (Barlow & Middleton 1990). If the bovine-to-human species barrier were similar to that for mice, it would suggest an oral LD 50 in humans of an order of magnitude also similar to that for mice (approximately 10 g). Clearly, it is hoped that the species barrier limiting transmission of BSE to humans will be of a far higher order. However, if we assume a pessimistic scenario, that the barrier is similar (and it remains possible it could be lower), extrapolation with the known incubation periods in the acquired human prion diseases, such as growth hormone-related iatrogenic CJD or kuru, where transmission does not involve a species barrier (and mean incubation periods are approximately 10-15 years), would suggest mean incubation periods of BSE in humans of perhaps 30 years or more, and a range extending from 10 years to, or exceeding, a normal human lifespan. Such estimations (Collinge 1999), based on extensive experience of transmission studies across species from many research groups over several decades, suggest-only 4 years after recognition of vCJD- the need for caution with respect to optimistic assessments of likely human BSE epidemic size.


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