Competition between Different Scrapie Agents in Mice

Dickinson, A. G.; Fraser, H.; Meikle, Veronica M. H.; Outram, G. W.

doi:10.1038/newbio237244a0

Cited by 102 publications

(75 citation statements)

References 4 publications

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“…route of inoculation. In previous studies with murine-adapted scrapie and Creutzfeldt-Jakob disease prions, the long-incubation-period prion strains could delay or block the short-incubation-period strains only if they were able to cause disease in the absence of superinfection (Dickinson et al, 1972(Dickinson et al, , 1975Kimberlin & Walker, 1985;Manuelidis, 1998;Manuelidis & Yun Lu, 2000). The current findings are paradoxical, since the DY TME agent does not cause TME or replicate in the LRS and nervous system following i.p.…”

Section: Parallels In Natural Bse In Which Prpcontrasting

confidence: 55%

“…superinfection) by intraperitoneal (i.p.) inoculation can result in murine scrapie strain 22A (a long-incubationperiod strain) blocking disease caused by scrapie strain 22C (a short-incubation-period strain) (Dickinson et al, 1972(Dickinson et al, , 1975. As a result, mice die from disease caused by 22A scrapie and there is no evidence of 22C scrapie infection in the brain.…”

Section: Introductionmentioning

confidence: 99%

“…Both a delay and a blocking effect on a fast prion strain by a slow prion strain have been reported following superinfection by the intracerebral (i.c.) route of inoculation (Dickinson et al, 1972;Manuelidis, 1998). In the former case, mice inoculated with 22A scrapie agent died from a subsequent 22C scrapie superinfection but the time to onset of disease was protracted compared with a control 22C scrapie infection (Dickinson et al, 1972).…”

Section: Introductionmentioning

confidence: 99%

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Delay in onset of prion disease for the HY strain of transmissible mink encephalopathy as a result of prior peripheral inoculation with the replication-deficient DY strain

Bartz

Aiken

Bessen

2004

Journal of General Virology

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We report that the replication-deficient DY strain of transmissible mink encephalopathy (TME) can delay disease caused by the pathogenic HY TME strain. In this study, competition between the HY and DY TME agents was investigated following superinfection of the sciatic nerve and peritoneal cavity. Initially, DY TME infection was examined in the absence of superinfection and it was found that inoculation into the brain and sciatic nerve resulted in prion disease and PrP Sc deposition in brain but not lymphoreticular tissues. Conversely, intraperitoneal inoculation of the DY TME agent did not result in clinical symptoms, DY TME agent replication or PrP Sc deposition 400-600 days after infection. These findings indicate that the DY TME agent does not replicate in secondary lymphoid organs and is non-pathogenic when neuroinvasion is dependent on prior infection of the lymphoreticular system. However, intraperitoneal inoculation of the DY TME agent at 60 days, but not at 30 days, prior to intraperitoneal inoculation of the HY TME agent resulted in an extension of the HY TME incubation period. Inoculation of the DY TME agent into the sciatic nerve at 60 days prior to intrasciatic nerve inoculation of the HY TME agent did not delay the incubation period of HY TME. The ability of the DY TME agent to delay HY TME infection following extraneural inoculation, but not neural infection, suggests that HY and DY TME agent competition can occur in a common replication site whose cellular location precedes infection of both the lymphoreticular and peripheral nervous systems.

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Section: Parallels In Natural Bse In Which Prpcontrasting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Delay in onset of prion disease for the HY strain of transmissible mink encephalopathy as a result of prior peripheral inoculation with the replication-deficient DY strain

Bartz

Aiken

Bessen

2004

Journal of General Virology

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“…10 Interference between other prion strains has been described in mice and hamsters using rodent-adapted strains of scrapie, TME, Creutzfeldt-Jacob disease and Gerstmannn-Sträussler-Scheinker syndrome following intracerebral, intraperitoneal, intravenous and sciatic nerve routes of inoculation. [10][11][12][13][14][15] We previously demonstrated the detection of PrP Sc from the long incubation period DY TME agent correlated with its ability to extend the incubation period or completely block the superinfecting short incubation period HY TME agent from causing disease and results in a reduction of HY PrP Sc levels following sciatic nerve inoculation. 12 However, it is not known if a single long incubation period agent (e.g., DY TME) can interfere with more than one short incubation period agent or if interference can occur by a natural route of infection.…”

mentioning

confidence: 99%

Prion interference with multiple prion isolates

Schutt

Bartz

2008

Prion

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“…This extension in incubation period is termed strain interference. Strain interference has been shown to occur in mice 10 and hamsters 22 . Bartz and co-workers have used PMCA to study prion strain interference in hamsters.…”

Section: Discussionmentioning

confidence: 99%

Protein Misfolding Cyclic Amplification of Prions

Saunders

Bartz

Shikiya

2012

JoVE

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Prions are infectious agents that cause the inevitably fatal transmissible spongiform encephalopathy (TSE) in animals and humans 9,18 . The prion protein has two distinct isoforms, the non-infectious host-encoded protein (PrP . This technique has proven to effectively recapitulate the species and strain specificity of PrP Sc conversion from PrP C , to emulate prion strain interference, and to amplify very low levels of PrP Sc from infected tissues, fluids, and environmental samples 6,7,16,23 . This paper details the PMCA protocol, including recommendations for minimizing contamination, generating consistent results, and quantifying those results. We also discuss several PMCA applications, including generation and characterization of infectious prion strains, prion strain interference, and the detection of prions in the environment. Video LinkThe video component of this article can be found at

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Competition between Different Scrapie Agents in Mice

Cited by 102 publications

References 4 publications

Delay in onset of prion disease for the HY strain of transmissible mink encephalopathy as a result of prior peripheral inoculation with the replication-deficient DY strain

Delay in onset of prion disease for the HY strain of transmissible mink encephalopathy as a result of prior peripheral inoculation with the replication-deficient DY strain

Prion interference with multiple prion isolates

Protein Misfolding Cyclic Amplification of Prions

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