title: Quantitative genetics of Taura syndrome resistance in Pacific white shrimp (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 21 separate 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.
authors.affiliation: Nofima Marin, NO-1432 Ås, Norway. jorgen.odegard@nofima.no
authors.forename: Jørgen
authors.initials: J
authors.lastname: Ødegård
authors.forename: Thomas
authors.initials: T
authors.lastname: Gitterle
authors.forename: Per
authors.initials: P
authors.lastname: Madsen
authors.forename: Theo H E
authors.initials: TH
authors.lastname: Meuwissen
authors.forename: M Hossein
authors.initials: MH
authors.lastname: Yazdi
authors.forename: Bjarne
authors.initials: B
authors.lastname: Gjerde
authors.forename: Carlos
authors.initials: C
authors.lastname: Pulgarin
authors.forename: Morten
authors.initials: M
authors.lastname: Rye
mesh_terms: D000818:Animals; D056629:Dicistroviridae / Q000235:genetics* / Q000302:isolation & purification; D020022:Genetic Predisposition to Disease; D033561:Penaeidae / Q000235:genetics* / Q000821:virology*; D010807:Physical Endurance / Q000502:physiology; D011153:Population; D012327:RNA Virus Infections / Q000235:genetics; D016019:Survival Analysis