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Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis
J C Bartz1, D I McKenzie, R A Bessen
1Department of Animal Health and Biomedical Sciences, University of Wisconsin, Madison 53706.
Abstract:
Experimental infection of transmissible mink encephalopathy (TME) in two closely related mustelids, black ferret (Mustela putorius furo) and mink (Mustela visa), revealed differences in their susceptibility to the TME agent. When challenged with the Stetsonville TME agent, a longer incubation period was observed in ferrets (28 to 38 months) than mink (4 months). Western blot analysis of ferret and mink prion proteins (PrP) demonstrated no detectable differences between the proteins. Northern blot analysis of ferret brain RNA indicated that PrP mRNA abundance is similar in infected and uninfected individuals. We amplified the PrP coding region from ferret DNA using the polymerase chain reaction and compared the deduced amino acid sequence of the ferret PrP gene with the mink PrP gene. This comparison revealed six silent base changes and two amino acid changes between mink and ferret: Phe-->Lys at codon 179 and Arg-->Gln at codon 224, respectively. These changes may indicate the region of PrP that is responsible for the species barrier effect between mink and ferret.
Insights
Transmissible mink encephalopathy (TME) affects ferrets and mink differently. Ferrets show longer incubation periods for TME, suggesting specific prion protein (PrP) gene variations influence disease susceptibility and the species barrier effect.
Area of Science:
- Neuroscience
- Veterinary Pathology
- Molecular Biology
Background:
- Transmissible mink encephalopathy (TME) is a prion disease affecting mustelids.
- Understanding species-specific susceptibility is crucial for prion disease research.
Purpose of the Study:
- To investigate the differences in susceptibility to the TME agent between black ferrets and mink.
- To identify potential genetic factors contributing to the observed species barrier effect.
Main Methods:
- Experimental infection of ferrets and mink with the Stetsonville TME agent.
- Western blot analysis of prion protein (PrP) in ferret and mink brains.
- Northern blot analysis of PrP mRNA abundance in ferret brains.
- Polymerase chain reaction (PCR) amplification and sequencing of the PrP coding region from ferret DNA.
Main Results:
- Ferrets exhibited significantly longer incubation periods (28-38 months) compared to mink (4 months) when experimentally infected with TME.
- Western blot analysis revealed no detectable differences in PrP between infected ferrets and mink.
- Northern blot analysis showed similar PrP mRNA abundance in infected and uninfected ferrets.
- Comparison of PrP genes identified six silent base changes and two amino acid alterations (Phe-->Lys at codon 179, Arg-->Gln at codon 224) between mink and ferret.
Conclusions:
- The study highlights distinct susceptibility levels to TME between ferrets and mink.
- Specific amino acid changes in the prion protein (PrP) gene may be responsible for the observed species barrier effect in TME.
- Further research into these PrP variations could elucidate mechanisms of prion disease transmission and host range.