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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Autores principales:	Debby Lipschutz-Powell, John A Woolliams, Piter Bijma, Andrea B Doeschl-Wilson
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/88729808fa7a4112864f791a066266e5
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spelling	oai:doaj.org-article:88729808fa7a4112864f791a066266e52021-11-18T07:13:57ZIndirect genetic effects and the spread of infectious disease: are we capturing the full heritable variation underlying disease prevalence?1932-620310.1371/journal.pone.0039551https://doaj.org/article/88729808fa7a4112864f791a066266e52012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22768088/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Reducing 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.Debby Lipschutz-PowellJohn A WoolliamsPiter BijmaAndrea B Doeschl-WilsonPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 6, p e39551 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q 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?
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.
format	article
author	Debby Lipschutz-Powell John A Woolliams Piter Bijma Andrea B Doeschl-Wilson
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)
publishDate	2012
url	https://doaj.org/article/88729808fa7a4112864f791a066266e5
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Indirect genetic effects and the spread of infectious disease: are we capturing the full heritable variation underlying disease prevalence?

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