Use of multi-trait and random regression models to identify genetic variation in tolerance to porcine reproductive and respiratory syndrome virus.
Use of multi-trait and random regression models to identify genetic variation in tolerance to porcine reproductive and respiratory syndrome virus.
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DOI：
10.1186/s12711-017-0312-7
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发表时间：
2017-04-19
期刊：
影响因子：
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通讯作者：
Doeschl-Wilson A
中科院分区：
文献类型：
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作者：
Lough G;Rashidi H;Kyriazakis I;Dekkers JCM;Hess A;Hess M;Deeb N;Kause A;Lunney JK;Rowland RRR;Mulder HA;Doeschl-Wilson A
宿主可以采取两种应对感染的策略：耐药性（减少病原体负荷）和耐受性（尽量减少感染对性能的影响）。这两种策略都可能受到遗传控制，因此可以作为遗传改良的目标。尽管有证据支持对猪繁殖与呼吸综合征（PRRS）的抗性存在遗传基础，但尚不清楚猪的耐受性是否也存在遗传差异。我们确定了猪对PRRS的抗性基因变异在多大程度上也表现出耐受性基因变异。采用多性状线性混合模型和随机回归父系模型拟合PRRS宿主遗传协会1320头断奶猪（54个父系的后代）的数据，以获得PRRS病毒毒株的抗性和耐受性的遗传参数估计。抗性定义为感染后0 ~ 21天（VL21）或0 ~ 42天（VL42）宿主内病毒载量（VL）的倒数，耐受性定义为VL21或VL42上平均日增重（ADG21、ADG42）反应规范的斜率。对ADG与低或高VL相关的多性状分析并不能表明耐受性的遗传变异。同样，ADG21和ADG42的随机回归模型对每一种母系的耐受性斜率进行拟合，结果并不比没有耐受性遗传变异的模型更适合数据。然而，平均VL附近的数据分布表明回归线的水平和斜率估计之间可能存在混淆。用未感染的同父异母兄弟姐妹（ADG0）的模拟生长速率增加数据有助于解决这一统计混淆，并表明如果ADG0与ADG21或ADG42之间的遗传相关性为低至中等，则可能存在对PRRS耐受性的遗传变异。当仅基于感染仔猪的数据时，猪对PRRS耐受性的遗传变异证据不足。然而，模拟结果表明，耐受性方面可能存在遗传差异，如果有未感染亲属的可比数据，就可以检测到这种差异。总之，在这两种防御策略中，耐受性的遗传比抗性的遗传更难以阐明。本文的在线版本（doi:10.1186/s12711-017-0312-7）包含补充材料，仅供授权用户使用。
A host can adopt two response strategies to infection: resistance (reduce pathogen load) and tolerance (minimize impact of infection on performance). Both strategies may be under genetic control and could thus be targeted for genetic improvement. Although there is evidence that supports a genetic basis for resistance to porcine reproductive and respiratory syndrome (PRRS), it is not known whether pigs also differ genetically in tolerance. We determined to what extent pigs that have been shown to vary genetically in resistance to PRRS also exhibit genetic variation in tolerance. Multi-trait linear mixed models and random regression sire models were fitted to PRRS Host Genetics Consortium data from 1320 weaned pigs (offspring of 54 sires) that were experimentally infected with a virulent strain of PRRS virus to obtain genetic parameter estimates for resistance and tolerance. Resistance was defined as the inverse of within-host viral load (VL) from 0 to 21 (VL21) or 0 to 42 (VL42) days post-infection and tolerance as the slope of the reaction-norm of average daily gain (ADG21, ADG42) on VL21 or VL42. Multi-trait analysis of ADG associated with either low or high VL was not indicative of genetic variation in tolerance. Similarly, random regression models for ADG21 and ADG42 with a tolerance slope fitted for each sire did not result in a better fit to the data than a model without genetic variation in tolerance. However, the distribution of data around average VL suggested possible confounding between level and slope estimates of the regression lines. Augmenting the data with simulated growth rates of non-infected half-sibs (ADG0) helped resolve this statistical confounding and indicated that genetic variation in tolerance to PRRS may exist if genetic correlations between ADG0 and ADG21 or ADG42 are low to moderate. Evidence for genetic variation in tolerance of pigs to PRRS was weak when based on data from infected piglets only. However, simulations indicated that genetic variance in tolerance may exist and could be detected if comparable data on uninfected relatives were available. In conclusion, of the two defense strategies, genetics of tolerance is more difficult to elucidate than genetics of resistance. The online version of this article (doi:10.1186/s12711-017-0312-7) contains supplementary material, which is available to authorized users.