Genetic analysis of vibriosis and viral nervous necrosis resistance in Atlantic cod (Gadus morhua L.) using a cure model1

Abstract

The aim of this study was to investigate whether observed time-until-death of Atlantic cod (Gadus morhua L.) juveniles in separate challenge tests with Vibrio anguillarum (causes vibriosis) and nodavirus [causes viral nervous necrosis (VNN)] are due to differences in susceptibility (whether at risk or not) or increased endurance (individual hazard, given that the animal is susceptible) using a cure mixture (CURE) model with Gibbs sampling. Observed time-until-death, prepared as sequential binary records, were analyzed with the CURE model and results were compared with cross-sectional threshold (SIMPLE) and an ordinary longitudinal survival score (NAÏVE) model (i.e., assuming that all animals are susceptible). Overall mortality at the end of the test was 86 and 71% for vibriosis and VNN, respectively. But the CURE model estimated 92 and 82% of the population to be susceptible to vibriosis and VNN, respectively. Hence, a substantial fraction among the survivors were considered to be susceptible but with high endurance. The underlying heritability of susceptibility was moderate for vibriosis (0.33) and extremely high for VNN (0.91), somewhat greater compared with classical SIMPLE model (0.19 and 0.76 for vibriosis and VNN, respectively), analyzing end survival as a cross-sectional binary trait. Estimates of the underlying heritability were low for single test-day scores of both endurance (0.02 and 0.15 for vibriosis and VNN, respectively) in the CURE model and for the NAÏVE model (0.02 and 0.18 for vibriosis and VNN, respectively). Based on the CURE model, the genetic correlation between susceptibility and endurance was low to moderately positive and significantly different from unity (P < 0.01) for both vibriosis (0.13) and VNN (0.47). Estimated breeding values from the SIMPLE and NAÏVE models showed moderate to high correlations (0.41 to 0.96) with EBV for susceptibility and endurance in the CURE model. The analyses indicate that susceptibility and endurance are apparently distinct genetic traits. Still, the genetic variation estimated in the SIMPLE and NAÏVE models seems to a large extent to be controlled by susceptibility and an efficient genetic selection for reduced susceptibility to vibriosis and VNN is therefore likely feasible even when using classical (noncure) models. Earlier termination of the challenge test or back truncation of survival data is not recommended as this likely shifts the focus of selection towards endurance rather than susceptibility.