Abstract
Biochemical and biophysical properties of prions including possible inactivation methods are reviewed. Possible molecular markers of transmissible spongiform encephalopathy (TSE) and mechanisms behind infectivity and correlation with clinical symptoms are discussed. The risk of Bovine Spongiform Encephalopathy (BSE) for humans i.e. variant Creutzfeldt–Jakob Disease (cCJD) is addressed in detail. The consequences of the emergence of the new cCJD and the lack of information on the infectivity of cCJD at the clinical stage of the disease in relation to the need to reconsider the biological concepts currently used in microbiology.
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