Why breed disease-resilient livestock, and how?

Why breed disease-resilient livestock, and how?
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为什么要培育对疾病有抵抗力的牲畜,以及如何培育?

DOI:
10.1186/s12711-020-00580-4
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发表时间:
2020-10-14
期刊:
Genetics, selection, evolution : GSE
影响因子:
--
通讯作者:
Doeschl-Wilson A
Doeschl-Wilson A
中科院分区:
其他
文献类型:
--
作者:
Knap PW;Doeschl-Wilson A

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防治流行病和地方病给畜牧业生产造成了相当大的损失。许多研究致力于培育抗病家畜,但这在实际育种计划中还不是一个共同的目标。在本文中,我们探讨了未来的育种计划如何受益于最近的疾病恢复力的研究。我们定义疾病的弹性在其组成性状的阻力(R:宿主动物的能力,以限制宿主内病原体负荷(PL))和耐受性(T:感染的主机,以限制由一个给定的PL造成的损害的能力),和模型主机的生产性能作为PL的反应规范,取决于R和T。在此基础上,我们推导出弹性及其组成性状的经济价值方程。一项关于猪呼吸和生殖综合征的案例研究表明,通过选择抗病和抗病品种在感染条件下提高产量的经济价值比选择无病条件下的产量高出三倍以上。虽然这种反应规范模型的弹性是有助于量化其关系的组成特征,其参数是困难和昂贵的量化。我们认为忽视的后果R和T的育种计划,衡量生产的弹性在感染性条件下与未知的PL,特别是风险,R和T之间的遗传相关性是不利的(拮抗),他们之间的权衡中和的弹性改善。我们描述了避免这种拮抗作用的四种方法:(1)通过产生足够的PL记录来估计这种相关性并检查拮抗作用-如果发现,则继续常规PL记录,如果没有发现,则转移到更便宜的PL替代物:(2)通过选择已知以有利方式影响R和T的数量性状位点(QTL);(3)通过快速修改接近完全的抵抗力或耐受性,(4)通过重新定义弹性作为动物抵抗(或恢复)由感染引起的干扰的能力,作为生产性状在宿主内纵向数据系列中的时间偏差来测量。所有四种替代方案都为从基因上改善疾病复原力提供了有希望的选择,而且大多数都依赖于技术和方法的发展以及自动数据生成方面的创新。
Fighting and controlling epidemic and endemic diseases represents a considerable cost to livestock production. Much research is dedicated to breeding disease resilient livestock, but this is not yet a common objective in practical breeding programs. In this paper, we investigate how future breeding programs may benefit from recent research on disease resilience. We define disease resilience in terms of its component traits resistance (R: the ability of a host animal to limit within-host pathogen load (PL)) and tolerance (T: the ability of an infected host to limit the damage caused by a given PL), and model the host's production performance as a reaction norm on PL, depending on R and T. Based on this, we derive equations for the economic values of resilience and its component traits. A case study on porcine respiratory and reproductive syndrome (PRRS) in pigs illustrates that the economic value of increasing production in infectious conditions through selection for R and T can be more than three times higher than by selection for production in disease-free conditions. Although this reaction norm model of resilience is helpful for quantifying its relationship to its component traits, its parameters are difficult and expensive to quantify. We consider the consequences of ignoring R and T in breeding programs that measure resilience as production in infectious conditions with unknown PL—particularly, the risk that the genetic correlation between R and T is unfavourable (antagonistic) and that a trade-off between them neutralizes the resilience improvement. We describe four approaches to avoid such antagonisms: (1) by producing sufficient PL records to estimate this correlation and check for antagonisms—if found, continue routine PL recording, and if not found, shift to cheaper proxies for PL; (2) by selection on quantitative trait loci (QTL) known to influence both R and T in favourable ways; (3) by rapidly modifying towards near-complete resistance or tolerance, (4) by re-defining resilience as the animal's capacity to resist (or recover from) the perturbation caused by an infection, measured as temporal deviations of production traits in within-host longitudinal data series. All four alternatives offer promising options for genetic improvement of disease resilience, and most rely on technological and methodological developments and innovation in automated data generation.
DOI: 10.3389/fgene.2020.00216
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DOI: 10.1186/1297-9686-46-18
发表时间: 2014-03-04
期刊: Genetics, selection, evolution : GSE
影响因子: --
作者:
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DOI: 10.1111/j.1461-0248.2004.00680.x
发表时间: 2004-12-01
期刊: ECOLOGY LETTERS
影响因子: 8.8
作者:
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通讯作者: Stinchcombe, JR
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影响因子: 3.5
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