Quantitative genetics of Taura syndrome resistance in Pacific (Penaeus vannamei): A cure model approach

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Quantitative genetics of Taura syndrome resistance in Pacific (Penaeus vannamei): A cure model approach. / Ødegård, Jørgen; Gitterle, Thomas; Madsen, Per; Meuwissen, Theo HE; Yazdi, M Hossein; Gjerde, Bjarne; Pulgarin, Carlos; Rye, Morten.

I: Genetics Selection Evolution, Bind 43, Nr. 14, 21.03.2011.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Ødegård, J, Gitterle, T, Madsen, P, Meuwissen, THE, Yazdi, MH, Gjerde, B, Pulgarin, C & Rye, M 2011, 'Quantitative genetics of Taura syndrome resistance in Pacific (Penaeus vannamei): A cure model approach', Genetics Selection Evolution, bind 43, nr. 14.

APA

Ødegård, J., Gitterle, T., Madsen, P., Meuwissen, T. HE., Yazdi, M. H., Gjerde, B., Pulgarin, C., & Rye, M. (2011). Quantitative genetics of Taura syndrome resistance in Pacific (Penaeus vannamei): A cure model approach. Genetics Selection Evolution, 43(14).

CBE

Ødegård J, Gitterle T, Madsen P, Meuwissen THE, Yazdi MH, Gjerde B, Pulgarin C, Rye M. 2011. Quantitative genetics of Taura syndrome resistance in Pacific (Penaeus vannamei): A cure model approach. Genetics Selection Evolution. 43(14).

MLA

Ødegård, Jørgen o.a.. "Quantitative genetics of Taura syndrome resistance in Pacific (Penaeus vannamei): A cure model approach". Genetics Selection Evolution. 2011. 43(14).

Vancouver

Ødegård J, Gitterle T, Madsen P, Meuwissen THE, Yazdi MH, Gjerde B o.a. Quantitative genetics of Taura syndrome resistance in Pacific (Penaeus vannamei): A cure model approach. Genetics Selection Evolution. 2011 mar 21;43(14).

Author

Ødegård, Jørgen ; Gitterle, Thomas ; Madsen, Per ; Meuwissen, Theo HE ; Yazdi, M Hossein ; Gjerde, Bjarne ; Pulgarin, Carlos ; Rye, Morten. / Quantitative genetics of Taura syndrome resistance in Pacific (Penaeus vannamei): A cure model approach. I: Genetics Selection Evolution. 2011 ; Bind 43, Nr. 14.

Bibtex

@article{e2d5256d55df47d89f1321e7e05b9971,
title = "Quantitative genetics of Taura syndrome resistance in Pacific (Penaeus vannamei): A cure model approach",
abstract = "Background: In aquaculture breeding, resistance against infectious diseases is commonly assessed as time until death under exposure to a pathogen. For some diseases, a fraction of the individuals may appear as “cured” (non-susceptible), and the resulting survival time may thus be a result of two confounded underlying traits, i.e., endurance (individual hazard) and susceptibility (whether at risk or not), which may be accounted for by fitting a cure survival model. We applied a cure model to survival data of Pacific white shrimp (Penaeus vannamei) challenged with the Taura syndrome virus, which is one of the major pathogens of Panaeid shrimp species. Methods: In total, 15,261 individuals of 513 full-sib families from three generations were challenge-tested in 21separate tests (tanks). All challenge-tests were run until mortality naturally ceased. Time-until-event data were analyzed with a mixed cure survival model using Gibbs sampling, treating susceptibility and endurance as separate genetic traits. Results: Overall mortality at the end of test was 28%, while 38% of the population was considered susceptible to the disease. The estimated underlying heritability was high for susceptibility (0.41 ± 0.07), but low for endurance (0.07 ± 0.03). Furthermore, endurance and susceptibility were distinct genetic traits (rg = 0.22 ± 0.25). Estimated breeding values for endurance and susceptibility were only moderately correlated (0.50), while estimated breeding values from classical models for analysis of challenge-test survival (ignoring the cured fraction) were closely correlated with estimated breeding values for susceptibility, but less correlated with estimated breeding values for endurance. Conclusions: For Taura syndrome resistance, endurance and susceptibility are apparently distinct genetic traits. However, genetic evaluation of susceptibility based on the cure model showed clear associations with standard genetic evaluations that ignore the cure fraction for these data. Using the current testing design, genetic variation in observed survival time and absolute survival at the end of test were most likely dominated by genetic variation in susceptibility. If the aim is to reduce susceptibility, earlier termination of the challenge-test or back-truncation of the follow-up period should be avoided, as this may shift focus of selection towards endurance rather than susceptibility.",
author = "J{\o}rgen {\O}deg{\aa}rd and Thomas Gitterle and Per Madsen and Meuwissen, {Theo HE} and Yazdi, {M Hossein} and Bjarne Gjerde and Carlos Pulgarin and Morten Rye",
year = "2011",
month = mar,
day = "21",
language = "English",
volume = "43",
journal = "Genetics Selection Evolution",
issn = "0999-193X",
publisher = "BioMed Central Ltd.",
number = "14",

}

RIS

TY - JOUR

T1 - Quantitative genetics of Taura syndrome resistance in Pacific (Penaeus vannamei): A cure model approach

AU - Ødegård, Jørgen

AU - Gitterle, Thomas

AU - Madsen, Per

AU - Meuwissen, Theo HE

AU - Yazdi, M Hossein

AU - Gjerde, Bjarne

AU - Pulgarin, Carlos

AU - Rye, Morten

PY - 2011/3/21

Y1 - 2011/3/21

N2 - Background: In aquaculture breeding, resistance against infectious diseases is commonly assessed as time until death under exposure to a pathogen. For some diseases, a fraction of the individuals may appear as “cured” (non-susceptible), and the resulting survival time may thus be a result of two confounded underlying traits, i.e., endurance (individual hazard) and susceptibility (whether at risk or not), which may be accounted for by fitting a cure survival model. We applied a cure model to survival data of Pacific white shrimp (Penaeus vannamei) challenged with the Taura syndrome virus, which is one of the major pathogens of Panaeid shrimp species. Methods: In total, 15,261 individuals of 513 full-sib families from three generations were challenge-tested in 21separate tests (tanks). All challenge-tests were run until mortality naturally ceased. Time-until-event data were analyzed with a mixed cure survival model using Gibbs sampling, treating susceptibility and endurance as separate genetic traits. Results: Overall mortality at the end of test was 28%, while 38% of the population was considered susceptible to the disease. The estimated underlying heritability was high for susceptibility (0.41 ± 0.07), but low for endurance (0.07 ± 0.03). Furthermore, endurance and susceptibility were distinct genetic traits (rg = 0.22 ± 0.25). Estimated breeding values for endurance and susceptibility were only moderately correlated (0.50), while estimated breeding values from classical models for analysis of challenge-test survival (ignoring the cured fraction) were closely correlated with estimated breeding values for susceptibility, but less correlated with estimated breeding values for endurance. Conclusions: For Taura syndrome resistance, endurance and susceptibility are apparently distinct genetic traits. However, genetic evaluation of susceptibility based on the cure model showed clear associations with standard genetic evaluations that ignore the cure fraction for these data. Using the current testing design, genetic variation in observed survival time and absolute survival at the end of test were most likely dominated by genetic variation in susceptibility. If the aim is to reduce susceptibility, earlier termination of the challenge-test or back-truncation of the follow-up period should be avoided, as this may shift focus of selection towards endurance rather than susceptibility.

AB - Background: In aquaculture breeding, resistance against infectious diseases is commonly assessed as time until death under exposure to a pathogen. For some diseases, a fraction of the individuals may appear as “cured” (non-susceptible), and the resulting survival time may thus be a result of two confounded underlying traits, i.e., endurance (individual hazard) and susceptibility (whether at risk or not), which may be accounted for by fitting a cure survival model. We applied a cure model to survival data of Pacific white shrimp (Penaeus vannamei) challenged with the Taura syndrome virus, which is one of the major pathogens of Panaeid shrimp species. Methods: In total, 15,261 individuals of 513 full-sib families from three generations were challenge-tested in 21separate tests (tanks). All challenge-tests were run until mortality naturally ceased. Time-until-event data were analyzed with a mixed cure survival model using Gibbs sampling, treating susceptibility and endurance as separate genetic traits. Results: Overall mortality at the end of test was 28%, while 38% of the population was considered susceptible to the disease. The estimated underlying heritability was high for susceptibility (0.41 ± 0.07), but low for endurance (0.07 ± 0.03). Furthermore, endurance and susceptibility were distinct genetic traits (rg = 0.22 ± 0.25). Estimated breeding values for endurance and susceptibility were only moderately correlated (0.50), while estimated breeding values from classical models for analysis of challenge-test survival (ignoring the cured fraction) were closely correlated with estimated breeding values for susceptibility, but less correlated with estimated breeding values for endurance. Conclusions: For Taura syndrome resistance, endurance and susceptibility are apparently distinct genetic traits. However, genetic evaluation of susceptibility based on the cure model showed clear associations with standard genetic evaluations that ignore the cure fraction for these data. Using the current testing design, genetic variation in observed survival time and absolute survival at the end of test were most likely dominated by genetic variation in susceptibility. If the aim is to reduce susceptibility, earlier termination of the challenge-test or back-truncation of the follow-up period should be avoided, as this may shift focus of selection towards endurance rather than susceptibility.

M3 - Journal article

VL - 43

JO - Genetics Selection Evolution

JF - Genetics Selection Evolution

SN - 0999-193X

IS - 14

ER -