Protecting effect of PrP codons M142 and K222 in goats orally challenged with bovine spongiform encephalopathy prions

C. Fast, W. Goldmann, P. Berthon, Kerstin Tauscher, O. Andréoletti, I. Lantier, C. Rossignol, A. Bossers, J.G. Jacobs, N. Hunter, Martin H. Groschup, F. Lantier, J.P.M. Langeveld*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

5 Citations (Scopus)

Abstract

Breeding towards genetic resistance to prion disease is effective in eliminating scrapie. In sheep, classical forms of scrapie have been eradicated almost completely in several countries by breeding programs using a prion protein (PrP) gene (PRNP) amino acid polymorphism. For goats, field and experimental studies have provided evidence for several amino acid polymorphisms that are associated with resistance to scrapie, but only limited data are available concerning the susceptibility of caprine PRNP genotypes to BSE. In this study, goat kids representing five PRNP genotypes based on three polymorphisms (M142, Q211 and K222 and the wild type I142, R211 and Q222) were orally challenged with bovine or goat BSE. Wild type goats were killed with clinical signs between 24-28 months post inoculation (mpi) to both challenges, and goats with genotype R/Q211 succumbed between 29-36 mpi. I/M142 goats developed clinical signs at 44-45 mpi and M/M142 goats remained healthy until euthanasia at 48 mpi. None of the Q/K222 goats showed definite clinical signs. Taken together the highest attack ratios were seen in wild type and R/Q211 goats, and the lowest in I/M142, M/M142 and Q/K222. In all genotype groups, one or more goats remained healthy within the incubation period in both challenges and without detectable PrP deposition in the tissues. Our data show that both the K222 and M142 polymorphisms lengthen the incubation period significantly compared to wild type animals, but only K222 was associated with a significant increase in resistance to BSE infection after oral exposure to both BSE sources.
Original languageEnglish
Article number52
JournalVeterinary Research
Volume48
Issue number1
DOIs
Publication statusPublished - 2017

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Bovine Spongiform Encephalopathy
bovine spongiform encephalopathy
Prions
prions
Goats
codons
Codon
goats
Scrapie
scrapie
Genotype
genetic polymorphism
genotype
Breeding
Prion Proteins
Amino Acids
protein deposition
Prion Diseases
amino acids
Wild Animals

Cite this

Fast, C., Goldmann, W., Berthon, P., Tauscher, K., Andréoletti, O., Lantier, I., ... Langeveld, J. P. M. (2017). Protecting effect of PrP codons M142 and K222 in goats orally challenged with bovine spongiform encephalopathy prions. Veterinary Research, 48(1), [52]. https://doi.org/10.1186/s13567-017-0455-0
Fast, C. ; Goldmann, W. ; Berthon, P. ; Tauscher, Kerstin ; Andréoletti, O. ; Lantier, I. ; Rossignol, C. ; Bossers, A. ; Jacobs, J.G. ; Hunter, N. ; Groschup, Martin H. ; Lantier, F. ; Langeveld, J.P.M. / Protecting effect of PrP codons M142 and K222 in goats orally challenged with bovine spongiform encephalopathy prions. In: Veterinary Research. 2017 ; Vol. 48, No. 1.
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title = "Protecting effect of PrP codons M142 and K222 in goats orally challenged with bovine spongiform encephalopathy prions",
abstract = "Breeding towards genetic resistance to prion disease is effective in eliminating scrapie. In sheep, classical forms of scrapie have been eradicated almost completely in several countries by breeding programs using a prion protein (PrP) gene (PRNP) amino acid polymorphism. For goats, field and experimental studies have provided evidence for several amino acid polymorphisms that are associated with resistance to scrapie, but only limited data are available concerning the susceptibility of caprine PRNP genotypes to BSE. In this study, goat kids representing five PRNP genotypes based on three polymorphisms (M142, Q211 and K222 and the wild type I142, R211 and Q222) were orally challenged with bovine or goat BSE. Wild type goats were killed with clinical signs between 24-28 months post inoculation (mpi) to both challenges, and goats with genotype R/Q211 succumbed between 29-36 mpi. I/M142 goats developed clinical signs at 44-45 mpi and M/M142 goats remained healthy until euthanasia at 48 mpi. None of the Q/K222 goats showed definite clinical signs. Taken together the highest attack ratios were seen in wild type and R/Q211 goats, and the lowest in I/M142, M/M142 and Q/K222. In all genotype groups, one or more goats remained healthy within the incubation period in both challenges and without detectable PrP deposition in the tissues. Our data show that both the K222 and M142 polymorphisms lengthen the incubation period significantly compared to wild type animals, but only K222 was associated with a significant increase in resistance to BSE infection after oral exposure to both BSE sources.",
author = "C. Fast and W. Goldmann and P. Berthon and Kerstin Tauscher and O. Andr{\'e}oletti and I. Lantier and C. Rossignol and A. Bossers and J.G. Jacobs and N. Hunter and Groschup, {Martin H.} and F. Lantier and J.P.M. Langeveld",
year = "2017",
doi = "10.1186/s13567-017-0455-0",
language = "English",
volume = "48",
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issn = "0928-4249",
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Fast, C, Goldmann, W, Berthon, P, Tauscher, K, Andréoletti, O, Lantier, I, Rossignol, C, Bossers, A, Jacobs, JG, Hunter, N, Groschup, MH, Lantier, F & Langeveld, JPM 2017, 'Protecting effect of PrP codons M142 and K222 in goats orally challenged with bovine spongiform encephalopathy prions', Veterinary Research, vol. 48, no. 1, 52. https://doi.org/10.1186/s13567-017-0455-0

Protecting effect of PrP codons M142 and K222 in goats orally challenged with bovine spongiform encephalopathy prions. / Fast, C.; Goldmann, W.; Berthon, P.; Tauscher, Kerstin; Andréoletti, O.; Lantier, I.; Rossignol, C.; Bossers, A.; Jacobs, J.G.; Hunter, N.; Groschup, Martin H.; Lantier, F.; Langeveld, J.P.M.

In: Veterinary Research, Vol. 48, No. 1, 52, 2017.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Protecting effect of PrP codons M142 and K222 in goats orally challenged with bovine spongiform encephalopathy prions

AU - Fast, C.

AU - Goldmann, W.

AU - Berthon, P.

AU - Tauscher, Kerstin

AU - Andréoletti, O.

AU - Lantier, I.

AU - Rossignol, C.

AU - Bossers, A.

AU - Jacobs, J.G.

AU - Hunter, N.

AU - Groschup, Martin H.

AU - Lantier, F.

AU - Langeveld, J.P.M.

PY - 2017

Y1 - 2017

N2 - Breeding towards genetic resistance to prion disease is effective in eliminating scrapie. In sheep, classical forms of scrapie have been eradicated almost completely in several countries by breeding programs using a prion protein (PrP) gene (PRNP) amino acid polymorphism. For goats, field and experimental studies have provided evidence for several amino acid polymorphisms that are associated with resistance to scrapie, but only limited data are available concerning the susceptibility of caprine PRNP genotypes to BSE. In this study, goat kids representing five PRNP genotypes based on three polymorphisms (M142, Q211 and K222 and the wild type I142, R211 and Q222) were orally challenged with bovine or goat BSE. Wild type goats were killed with clinical signs between 24-28 months post inoculation (mpi) to both challenges, and goats with genotype R/Q211 succumbed between 29-36 mpi. I/M142 goats developed clinical signs at 44-45 mpi and M/M142 goats remained healthy until euthanasia at 48 mpi. None of the Q/K222 goats showed definite clinical signs. Taken together the highest attack ratios were seen in wild type and R/Q211 goats, and the lowest in I/M142, M/M142 and Q/K222. In all genotype groups, one or more goats remained healthy within the incubation period in both challenges and without detectable PrP deposition in the tissues. Our data show that both the K222 and M142 polymorphisms lengthen the incubation period significantly compared to wild type animals, but only K222 was associated with a significant increase in resistance to BSE infection after oral exposure to both BSE sources.

AB - Breeding towards genetic resistance to prion disease is effective in eliminating scrapie. In sheep, classical forms of scrapie have been eradicated almost completely in several countries by breeding programs using a prion protein (PrP) gene (PRNP) amino acid polymorphism. For goats, field and experimental studies have provided evidence for several amino acid polymorphisms that are associated with resistance to scrapie, but only limited data are available concerning the susceptibility of caprine PRNP genotypes to BSE. In this study, goat kids representing five PRNP genotypes based on three polymorphisms (M142, Q211 and K222 and the wild type I142, R211 and Q222) were orally challenged with bovine or goat BSE. Wild type goats were killed with clinical signs between 24-28 months post inoculation (mpi) to both challenges, and goats with genotype R/Q211 succumbed between 29-36 mpi. I/M142 goats developed clinical signs at 44-45 mpi and M/M142 goats remained healthy until euthanasia at 48 mpi. None of the Q/K222 goats showed definite clinical signs. Taken together the highest attack ratios were seen in wild type and R/Q211 goats, and the lowest in I/M142, M/M142 and Q/K222. In all genotype groups, one or more goats remained healthy within the incubation period in both challenges and without detectable PrP deposition in the tissues. Our data show that both the K222 and M142 polymorphisms lengthen the incubation period significantly compared to wild type animals, but only K222 was associated with a significant increase in resistance to BSE infection after oral exposure to both BSE sources.

UR - https://doi.org/10.6084/m9.figshare.c.3883954

U2 - 10.1186/s13567-017-0455-0

DO - 10.1186/s13567-017-0455-0

M3 - Article

VL - 48

JO - Veterinary Research

JF - Veterinary Research

SN - 0928-4249

IS - 1

M1 - 52

ER -