Indirect genetic effects and the spread of infectious disease: are we capturing the full heritable variation underlying disease prevalence?

Reducing disease prevalence through selection for host resistance offers a desirable alternative to chemical treatment. Selection for host resistance has proven difficult, however, due to low heritability estimates. These low estimates may be caused by a failure to capture all the relevant genetic v...

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Main Authors: Debby Lipschutz-Powell, John A Woolliams, Piter Bijma, Andrea B Doeschl-Wilson
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS ONE
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22768088/pdf/?tool=EBI
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spelling doaj-88729808fa7a4112864f791a066266e52021-03-04T12:37:32ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0176e3955110.1371/journal.pone.0039551Indirect genetic effects and the spread of infectious disease: are we capturing the full heritable variation underlying disease prevalence?Debby Lipschutz-PowellJohn A WoolliamsPiter BijmaAndrea B Doeschl-WilsonReducing disease prevalence through selection for host resistance offers a desirable alternative to chemical treatment. Selection for host resistance has proven difficult, however, due to low heritability estimates. These low estimates may be caused by a failure to capture all the relevant genetic variance in disease resistance, as genetic analysis currently is not taylored to estimate genetic variation in infectivity. Host infectivity is the propensity of transmitting infection upon contact with a susceptible individual, and can be regarded as an indirect effect to disease status. It may be caused by a combination of physiological and behavioural traits. Though genetic variation in infectivity is difficult to measure directly, Indirect Genetic Effect (IGE) models, also referred to as associative effects or social interaction models, allow the estimation of this variance from more readily available binary disease data (infected/non-infected). We therefore generated binary disease data from simulated populations with known amounts of variation in susceptibility and infectivity to test the adequacy of traditional and IGE models. Our results show that a conventional model fails to capture the genetic variation in infectivity inherent in populations with simulated infectivity. An IGE model, on the other hand, does capture some of the variation in infectivity. Comparison with expected genetic variance suggests that there is scope for further methodological improvement, and that potential responses to selection may be greater than values presented here. Nonetheless, selection using an index of estimated direct and indirect breeding values was shown to have a greater genetic selection differential and reduced future disease risk than traditional selection for resistance only. These findings suggest that if genetic variation in infectivity substantially contributes to disease transmission, then breeding designs which explicitly incorporate IGEs might help reduce disease prevalence.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22768088/pdf/?tool=EBI
collection DOAJ
language English
format Article
sources DOAJ
author Debby Lipschutz-Powell
John A Woolliams
Piter Bijma
Andrea B Doeschl-Wilson
spellingShingle Debby Lipschutz-Powell
John A Woolliams
Piter Bijma
Andrea B Doeschl-Wilson
Indirect genetic effects and the spread of infectious disease: are we capturing the full heritable variation underlying disease prevalence?
PLoS ONE
author_facet Debby Lipschutz-Powell
John A Woolliams
Piter Bijma
Andrea B Doeschl-Wilson
author_sort Debby Lipschutz-Powell
title Indirect genetic effects and the spread of infectious disease: are we capturing the full heritable variation underlying disease prevalence?
title_short Indirect genetic effects and the spread of infectious disease: are we capturing the full heritable variation underlying disease prevalence?
title_full Indirect genetic effects and the spread of infectious disease: are we capturing the full heritable variation underlying disease prevalence?
title_fullStr Indirect genetic effects and the spread of infectious disease: are we capturing the full heritable variation underlying disease prevalence?
title_full_unstemmed Indirect genetic effects and the spread of infectious disease: are we capturing the full heritable variation underlying disease prevalence?
title_sort indirect genetic effects and the spread of infectious disease: are we capturing the full heritable variation underlying disease prevalence?
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2012-01-01
description Reducing disease prevalence through selection for host resistance offers a desirable alternative to chemical treatment. Selection for host resistance has proven difficult, however, due to low heritability estimates. These low estimates may be caused by a failure to capture all the relevant genetic variance in disease resistance, as genetic analysis currently is not taylored to estimate genetic variation in infectivity. Host infectivity is the propensity of transmitting infection upon contact with a susceptible individual, and can be regarded as an indirect effect to disease status. It may be caused by a combination of physiological and behavioural traits. Though genetic variation in infectivity is difficult to measure directly, Indirect Genetic Effect (IGE) models, also referred to as associative effects or social interaction models, allow the estimation of this variance from more readily available binary disease data (infected/non-infected). We therefore generated binary disease data from simulated populations with known amounts of variation in susceptibility and infectivity to test the adequacy of traditional and IGE models. Our results show that a conventional model fails to capture the genetic variation in infectivity inherent in populations with simulated infectivity. An IGE model, on the other hand, does capture some of the variation in infectivity. Comparison with expected genetic variance suggests that there is scope for further methodological improvement, and that potential responses to selection may be greater than values presented here. Nonetheless, selection using an index of estimated direct and indirect breeding values was shown to have a greater genetic selection differential and reduced future disease risk than traditional selection for resistance only. These findings suggest that if genetic variation in infectivity substantially contributes to disease transmission, then breeding designs which explicitly incorporate IGEs might help reduce disease prevalence.
url https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22768088/pdf/?tool=EBI
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