Nature of the Scrapie Agent

Gibbons, R. A.; Hunter, G. D.

doi:10.1038/2151041a0

Cited by 164 publications

(61 citation statements)

References 26 publications

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“…The unusual properties of the scrapie agent, such as resistance to UV light, partial resistance to proteinase K (PK), high-pressure treatment, and high temperature, led to speculations that it might consist of protein only (44), or be devoid of both nucleic acid and protein (45), or be a polysaccharide (46) or a membrane fragment (47).…”

Section: Models Describing the Nature Of The Prion Protein And Its Rementioning

confidence: 99%

Molecular Mechanisms of Prion Pathogenesis

Aguzzi¹,

Sigurdson²,

Heikenwälder³

2007

Annu. Rev. Pathol. Mech. Dis.

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Section: Models Describing the Nature Of The Prion Protein And Its Rementioning

confidence: 99%

Molecular Mechanisms of Prion Pathogenesis

Aguzzi¹,

Sigurdson²,

Heikenwälder³

2007

Annu. Rev. Pathol. Mech. Dis.

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“…It seemed to me that the most intriguing question was the chemical nature of the scrapie agent; Alper's data had evoked a torrent of hypotheses concerning its composition. Suggestions as to the nature of the scrapie agent ranged from small DNA viruses to membrane fragments to polysaccharides to proteins, the last of which eventually proved to be correct (36)(37)(38)(39)(40)(41)(42).…”

mentioning

confidence: 99%

Molecular characterization of proteolytic cleavage sites of the Pseudomonas syringae effector AvrRpt2

Chisholm

Dahlbeck

Krishnamurthy

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

137

138

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Prions are unprecedented infectious pathogens that cause a group of invariably fatal neurodegenerative diseases by an entirely novel mechanism. Prion diseases may present as genetic, infectious, or sporadic disorders, all of which involve modification of the prion protein (PrP). Bovine spongiform encephalopathy (BSE), scrapie of sheep, and Creutzfeldt-Jakob disease (CJD) of humans are among the most notable prion diseases. Prions are transmissible particles that are devoid of nucleic acid and seem to be composed exclusively of a modified protein (PrP Sc ). The normal, cellular PrP (PrP C ) is converted into PrP Sc through a posttranslational process during which it acquires a high ␤-sheet content. The species of a particular prion is encoded by the sequence of the chromosomal PrP gene of the mammals in which it last replicated. In contrast to pathogens carrying a nucleic acid genome, prions appear to encipher strain-specific properties in the tertiary structure of PrP Sc . Transgenetic studies argue that PrP Sc acts as a template upon which PrP C is refolded into a nascent PrP Sc molecule through a process facilitated by another protein. Miniprions generated in transgenic mice expressing PrP, in which nearly half of the residues were deleted, exhibit unique biological properties and should facilitate structural studies of PrP Sc . While knowledge about prions has profound implications for studies of the structural plasticity of proteins, investigations of prion diseases suggest that new strategies for the prevention and treatment of these disorders may also find application in the more common degenerative diseases.

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“…The non-nucleic acid scrapie theory has been suggested since 1959 from several authors based on different properties (Stamp et al, 1959;Field, 1966;Alper et al, 1966Alper et al, , 1967Alper et al, , 1978Gibbons & Hunter, 1967). Although, at present, it is difficult to conceive a replicating molecule other than a nucleic acid, the possibility of new forms of replication must remain open.…”

Section: Discussionmentioning

confidence: 99%

Inability to Transmit Scrapie by Transfection of Mouse Embryo Cells in vitro

Dt²,

et al. 1982

Journal of General Virology

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SUMMARYInfectivity of nucleic acid from highly infectious mouse scrapie brains was studied by transfecting the nucleic acid in vitro prior to inoculation into animals. Foetal mouse brain and whole mouse embryo cultures were chosen as the cells used for the transfection. As an internal control, infectious nucleic acid was recovered from bacteriophage ~X174 and whole virus particles were obtained when cultures were transfected with herpes simplex virus DNA. In contrast, none of the animals inoculated with nucleic acid preparations derived from scrapie-infected tissues developed scrapie disease either with or without transfection procedures. These findings (i) show transfection techniques fail to elicit evidence of a scrapie-specific infectious nucleic acid and (ii) confirm the observation that scrapie is not a viroid.

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Nature of the Scrapie Agent

Cited by 164 publications

References 26 publications

Molecular Mechanisms of Prion Pathogenesis

Molecular Mechanisms of Prion Pathogenesis

Molecular characterization of proteolytic cleavage sites of the Pseudomonas syringae effector AvrRpt2

Inability to Transmit Scrapie by Transfection of Mouse Embryo Cells in vitro

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