Doeschl-Wilson, A. B. | Search bioRxiv

bioRxiv2018

Genetic differences in host infectivity affect disease spread and survival in epidemics

Survival during an epidemic is partly determined by host genetics. While quantitative genetic studies typically consider survival as an indicator for disease resistance, mortality rates of populations undergoing an epidemic are also affected by tolerance and infectivity (i.e. the propensity of an infected individual to transmit disease). Few studies have demonstrated genetic variation in disease tolerance, and no study has demonstrated genetic variation in host infectivity, despite strong evidence for considerable phenotypic variation in this trait. Here we propose an experimental design and statistical models for estimating genetic diversity in all three host traits. Using an infection model in fish we provide, for the first time, direct evidence for genetic variation in host infectivity, in addition to variation in resistance and tolerance. We also demonstrate how genetic differences in these three traits contribute to survival. Our results imply that animals can evolve different disease response types affecting epidemic survival rates, with important implications for understanding and controlling epidemics.

genetics↗

bioRxiv2018

Novel insights into the genetic relationship between growth and disease resistance in Pacific salmon

BackgroundBreeding for disease resistance has become a highly desirable strategy for mitigating infectious disease problems in aquaculture. However, knowledge of the genetic relationship between resistance and other economically important traits, such as growth, is important to assess prior to including disease resistance into the breeding goal. Our study assessed the genetic correlations between growth and survival traits in a large bacterial infection challenge experiment. A population of 2,606 coho salmon individuals from 107 full-sibling families were challenged with the bacteria Piscirickettsia salmonis. Growth was measured as average daily gain prior (ADG0) and during (ADGi) the experimental infection and as harvest weight (HW). Resistance was measured as Survival time (ST) and binary survival (BS). Furthermore, individual measures of bacterial load (BL) were assessed as new resistance phenotypes and to provide an indication of genetic variation in tolerance in salmonid species.\n\nResultsSignificant moderate heritabilities were estimated for ADG0 (0.30 {+/-} 0.05), HW (0.38 {+/-} 0.03), and for the survival traits ST (0.16 {+/-} 0.03) and BS (0.18 {+/-} 0.03). In contrast, heritabilities for ADGi and log-transformed BL were low (0.07 {+/-} 0.02 (significant) and 0.04 {+/-} 0.03, respectively), although these increased to moderate significant levels (0.20 {+/-} 0.09 and 0.12 {+/-} 0.05, respectively) when traits were assessed in survivors only. Significant and favorable genetic correlations were found between ADG0 and the growth traits ADGi (0.40 {+/-} 0.16) and HW (0.64 {+/-} 0.09), as well as with resistance as ST (0.43 {+/-} 0.18), indicating that fish with higher genetic growth rate early on and prior to infection not only tend to maintain their genetic growth advantage until harvest, but also tend to grow faster and survive longer during infection. Furthermore, no robust unfavorable genetic correlations between ADG0 and any of the other traits considered in this study, in particular BL, was identified. Adding log BL as covariates into the models for growth under infection and survival provided an indication for genetic variation in tolerance.\n\nConclusionsThese results suggest that selective breeding for early growth would be expected to simultaneously increase survival time and growth performance during an infection with Piscirickettsia salmonis after accounting for variation in bacterial load, and harvest weight in this coho salmon population, without negatively impacting on pathogen burden.

genetics↗