Abstract
The nature of the infective process in the transmissible spongiform encephalopathy (SE) diseases has been a longstanding problem — in particular, whether the causative agents are (unusual) nucleic-acid-mediated viruses, or replicating non-nucleic acid molecules such as protein. Although there is much (conflicting) evidence supporting both views, it does not seem to have been considered that many of the outstanding problems could be resolved if both mechanisms are operating — either separately or together — i.e. that there is a dual, but interconnected, pathway leading to disease development. It is suggested that this is in fact the case, and the implications are discussed.
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