Summary
The effects of disease, particularly when congenitally transmitted, on variance components and heritability were studied. Observations on lymphoid leukosis, a congenitally transmitted, viral disease of chickens, were used as the basis of the considerations but the results are deemed applicable to other situations where a population is similarly affected by a disease or another factor resulting in alteration of performance.
The numbers of pullets tested for lymphoid leukosis virus (LLV) shedding into eggs were 1785 in 1976 and 1699 in 1977. A comparison of the distribution of LLV shedders (approximately 8% of the birds tested) among sire and dam families with its binomial expectations supported earlier reports that only dams play a role in congenital transmission of LLV.
The effects of LLV infection on variance components and heritability were assessed in the 1976 data by comparing estimates from both LLV-shedders and nonshedders (population A) with estimates from nonshedders only (population B). Sire variances for age at first egg, number of eggs per hen housed, egg production rate, and egg weight were 3 to 18% greater in population A compared to population B. The corresponding differences in dam variances were generally larger (5 to 48%) while relative differences in individual variances were small (1 to 10%). Total phenotypic variances for the traits were 2 to 13% larger in population A than B. Corresponding changes in percent sire heritability ranged from −1 to 6%, and in dam heritability from −2 to 12%. The significance of these effects was not established with certainty due to standard errors of the estimates (9 to 13%). The study pointed out the need to consider possible effects of agents such as LLV on designing breeding plans, experiments and in data analyses.
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Communicated by H. Aplanalp
Animal Research Centre Contribution No. 1011
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Gavora, J.S., Chesnais, J. & Spencer, J.L. Estimation of variance components and heritability in populations affected by disease: lymphoid leukosis in chickens. Theoret. Appl. Genetics 65, 317–322 (1983). https://doi.org/10.1007/BF00276571
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DOI: https://doi.org/10.1007/BF00276571