Genetic relationships of antibody response, viremia level, and weight gain in pigs experimentally infected with porcine reproductive and respiratory syndrome virus1

• Published in: Journal of animal science 2018-09, Vol.96 (9), p.3565-3581
• Main Authors: Hess, Andrew S, Trible, Ben R, Hess, Melanie K, Rowland, Raymond R, Lunney, Joan K, Plastow, Graham S, Dekkers, Jack C M
• Format: Article
• Language: English
• Subjects: Animal Genetics and Genomics; Animals; Antibodies, Viral - genetics; Antibody Formation; Gene Expression Regulation; Genome; Genome-Wide Association Study; Genomics; Genotype; Polymorphism, Single Nucleotide; Porcine Reproductive and Respiratory Syndrome - genetics; Porcine respiratory and reproductive syndrome virus - immunology; Swine - growth & development; Swine - immunology; Viral Load - veterinary; Viremia; Weight Gain - genetics
• ISSN: 0021-8812; 1525-3163
• DOI: 10.1093/jas/sky229

Abstract Genetic and antigenic variability between Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) isolates has encumbered vaccine development. Here, the genetic basis of PRRSV antibody response was assessed using data from experimental infection trials of commercial crossbred weaner pigs across with one of two distinct PRRSV isolates, NVSL-97–7895 (~750 pigs) and KS-2006–72109 (~450 pigs). Objectives were to estimate the genetic parameters of antibody response, measured as the sample to positive ratio (S:P) of PRRSV N-protein specific IgG in serum at 42 d post infection (dpi); assess the relationship of S:P at 42 dpi with serum viremia and growth under infection; and identify genomic regions associated with S:P at 42 dpi. Estimates of heritability of S:P at 42 dpi for NVSL and KS06 were 0.31 ± 0.09 and 0.40 ± 0.10 and appeared to be under similar genetic control (genetic correlation 0.73 ± 0.39). Estimates of genetic correlations of S:P were generally weak with viral load (NVSL: −0.20 ± 0.18; KS06: −0.69 ± 0.20), measured as area under the curve of log10 serum viremia from 0 to 21 dpi, and with weight gain (WG) from 0 to 42 dpi (NVSL: −0.38 ± 0.19; KS06: −0.08 ± 0.25). However, genetic correlations of S:P at 42 dpi with daily serum viremia and with 3-d WG revealed dynamic relationships, with S:P at 42 dpi having the strongest negative genetic correlations with daily viremia when IgG production starts (10–20 dpi), and negative genetic correlations with WG early after infection but positive later on. This suggests that animals that placed more emphasis on immune response early in infection reaped benefits of that later in infection by more effectively clearing the virus. The WUR10000125 SNP on SSC4, previously associated with response to PRRSV, did not have a significant effect on S:P at 42 dpi (P > 0.05) but genotype-specific genetic correlations of S:P with daily viremia and 3-d WG suggested that the lower WG of pigs with the unfavorable AA WUR10000125 genotype may be due to their utilization of a more energetically costly host response compared to pigs with the favorable genotype. Genome-wide association studies identified three SNPs in the Major Histocompatibility Complex associated with S:P that explained ~10 (NVSL) and 45% (KS06) of the genetic variance but were not associated with viremia or WG. In conclusion, antibody response to PRRSV infection is a possible biomarker for improved host response to PRRSV infection.