[Models of the cause of spongiform encephalopathies].

Transmissible spongiform encephalopathies seem to contradict a dogma in microbiology. There is now increasing evidence that the infectious agents are proteins (prion proteins). These proteins seem to be able to catalyze conformational conversions of a host-encoded isoform. The altered conformation induces intracellular accumulation and may lead to polymerization into fibrils and amyloid rods. Catalytical interactions of infectious prion proteins and their cellular isoforms are dependent on the primary structure. These considerations may be helpful to evaluate the risk of transmission of BSE to humans.