Koch's postulates and infectious proteins

• Authors: Lary Walker, Emory University; Harry LeVine, University of Kentucky; Mathias Jucker, University of Tübingen
• Journal Title: ACTA NEUROPATHOLOGICA
• Volume: Volume 112, Number 1
• Publisher: SPRINGER | 2006-07-01, Pages 1-4
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1007/s00401-006-0072-x
• Subjects: Chemistry, Biochemistry
• Keywords: Science & Technology; Life Sciences & Biomedicine; Clinical Neurology; Neurosciences; Pathology; Neurosciences & Neurology; Alzheimer's disease; amyloid; apolipoprotein AII; conformational disease; prion; TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES; PRION DISEASES; NEURODEGENERATIVE DISORDERS; SPONTANEOUS GENERATION; FIBRIL CONFORMATION; SEEDING SPECIFICITY; AMYLOID FIBRILS; IN-VITRO; MECHANISM; PROPAGATION

Abstract

Koch's postulates were formulated in the late nineteenth century as guidelines for establishing that microbes cause specific diseases. Because the rules were developed for living agents - particularly bacteria - their applicability to inanimate pathogens such as viruses and infectious proteins has been problematic. The unorthodox mechanism by which prion diseases are transmitted, involving specific physicochemical characteristics of the protein as well as susceptibility traits of the host, has made these disorders refractory to analysis within the context of the original Koch's postulates. In addition, evidence is accumulating that other proteopathies, such as AA amyloidosis, apolipoprotein AII amyloidosis, and cerebral Aβ amyloidosis, can be induced in vulnerable recipients by cognate proteinaceous agents. In light of the salient differences in the mode of disease-transmission by microbes and proteins, we propose modifications of Koch's postulates that will specifically accommodate presumed infectious proteins. © Springer-Verlag 2006.