Abstract

The objective was to estimate genetic and environmental effects on PCVAD Score, anti-PCV2 IgG, PCV2 viremia, weight at birth, weaning, 65 d, and 180 d, and estimate correlations between traits. Pigs (n = 3,271) from Generations 24-26 of two lines selected for increased reproduction and growth and two control lines were scored as uninfected (0) or infected (1) for PCVAD. Overall, 14.4% of the pigs were scored as infected for PCVAD. Serum was collected at 60, 90, and 125 d of age from Generations 25 and 26 pigs. Body weights and anti-PCV2 IgG at 60 (IgG60, n = 799), 90 (IgG90, n = 773), and 125 d (IgG125, n = 684) of age were analyzed with ASREML assuming normality. PCVAD Score and viremia as a binomial trait (zero vs. non-zero) at 90 and 125 d of age were analyzed using a binomial distribution with the probit link. Non-zero viremia at 90 (V90, n = 469) and 125 d (V125, n = 536) of age were analyzed with a log₁₀-normal distribution. Direct heritabilities for PCVAD Score, weight at birth, weaning, 65 d, and 180 d, V90, V125, IgG90, and IgG125 were 0.16, 0.27, 0.16, 0.23, 0.23, 0.38, 0.11, 0.55, and 0.10, respectively. The proportion of variation due to environmental effects of contemporary group within generation, location, and finishing pen for PCVAD Score were 0.11, 0.22, and 0.05, respectively. The common environmental effect of the birth dam for IgG60, IgG90, and IgG125 were 0.58, 0.38, and 0.06, respectively. Direct genetic correlations of PCVAD Score with 65 d weight, V90, and IgG90 were -0.53, 0.75, and -0.67, respectively; 180 d weight with IgG90, V90, and V125 were 0.63, -0.48, and -0.80, respectively; IgG90 and V90 was -0.51; and V125 with 65 d weight was -0.73. Males had a significantly higher probability of PCVAD Score than females (P < 0.001). The results suggest genetics, sex, environment, antibodies, and viremia play a role in incidence of PCVAD.

Key Words: Pig, Genetic Variation, PCVAD