Animal TSEs and public health: What remains of past lessons?

Transmissible spongiform encephalopathies (TSEs) or prion diseases of animals include scrapie in sheep and goat, chronic wasting disease (CWD) in cervids (including mule deer, whitetailed deer, moose, elk, and reindeer), and bovine spongiform encephalopathy (BSE) in cattle; these diseases are either classical/naturally occurring or atypical forms and are thought to be caused by the spontaneous misfolding of prion protein.Marked heterogeneity with respect to clinicopathological features, susceptibility, and infectivity is known across and within the species, but the molecular basis for that phenomenon is still not completely understood, except for some factors.In most species, susceptibility to the disease is strongly influenced by the polymorphism in prion protein encoding gene (PRNP).In humans, the dimorphism at PRNP codon 129 (substitution of valine for methionine) impacts both the susceptibility and the phenotypes of TSEs [1].However, sheep with Q171R genotype show maximum resistance, and A136V genotype animals show maximum susceptibility to develop scrapie [2], and a single amino acid modification alters TSEs cross-species transmissions [3].Concerns and speculation about cross-species transmission of TSEs-particularly transmission of animal TSEs to humans-have existed since the infectious nature of these diseases was demonstrated, but there was no evidence of zoonotic transmission until the link between BSE and a novel human TSE (variant CJD or vCJD) was established in the late 1990s.While the number of vCJD clinical cases identified so far remains low, several studies suggested that 1 out of 2,000 individuals could be vCJD infected but asymptomatic in the United Kingdom population [4].In Europe, the emergence of vCJD triggered a major sanitary crisis that resulted in the implementation of a strong and coherent policy (EU regulation 999/2001) that aimed at eradicating animal TSEs.As a consequence of this policy, the BSE epidemic has nearly faded, and the EU authorities started to dismantle this policy.This change in the EU TSE doctrine raises questions about the necessity and the means to effectively protect human consumers from exposure to animals' prions. Cattle BSEsClassical BSE (C-BSE) was first recognized in 1984-85 as novel TSE affecting cattle in the UK [5].The epidemics caused about 180,000 clinical cases, and it was estimated that about 400,000 infected animals might have entered the food chain.BSE cases have been identified in Europe and in many other countries including United States of America, Canada, and Japan (Fig 1A & 1B).The National CJD Surveillance Unit UK has estimated that over 1 million infected cattle entered the human food chain [6].The origin of the BSEs has still not been clearly established, but the number of cases was amplified by the recycling of animal carcasses into cattle feed [7].The overwhelming weight of

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