|Knowles Jr, Donald|
Submitted to: Genetics Selection Evolution
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/22/2009
Publication Date: 1/22/2009
Citation: Harrington, R.D., Hoesing, L.M., White, S.N., Orourke, K.I., Knowles Jr, D.P. 2009. Ovine progressive pneumonia provirus levels are unaffected by the prion 171R allele in an Idaho sheep flock. Genetics Selection Evolution. 41(1):17
Interpretive Summary: Genetic selection of sheep for arginine at codon 171 of the prion gene confers resistance to scrapie. A possible effect of breeding for prion resistance upon other traits is uncertain. A possible association with ovine progressive pneumonia virus was investigated. Proviral levels were evaluated by quantitative PCR and compared for association with prion genotype by logistical regression modeling. It was found that ovine progressive pneumonia status and proviral levels were independent of the prion 171R allele. This study supports the use of codon 171 arginine breeding programs for control of scrapie.
Technical Abstract: Selective breeding of sheep for arginine (R) at prion gene (PRNP) codon 171 confers resistance to Scrapie. The 171R allele naturally occurs at low frequency, possibly because it imparts a deleterious trait such as impaired disease resistance. Ovine Progressive Pneumonia/Maedi-Visna virus (OPPV) is the primary economically important infection of sheep. If 171R selection affects OPPV it could significantly impact the sheep industry. A hypothesis that the PRNP 171R allele is associated with positive OPPV infection and higher OPPV proviral load was tested in an Idaho sheep flock using a logistical regression model that included breed, age, and interaction between breed and age as variables. OPPV provirus was found in 226 of 358 sheep by quantitative PCR. The frequency of OPPV positive animals did not differ significantly between the 171QQ, 171QR, and 171RR genotypes (p>0.05). OPPV proviral load levels of infected sheep were not significantly different among codon 171 genotypes (p>0.05). A minor allele at codon 143 was also examined. OPPV status and OPPV proviral load were statistically equivalent between 143 HH and 143 HR genotypes (p>0.05). This experiment shows that, in the flock examined, OPPV infection status and proviral load are independent of the PRNP 171R and 143R alleles. These results indicate that a genetic approach to Scrapie control is not expected to impact host resistance to OPPV and supports the adoption of PRNP 171R selection as a Scrapie control measure.