Degree Type

Dissertation

Date of Award

2016

Degree Name

Doctor of Philosophy

Department

Animal Science

Major

Genetics

First Advisor

Jack C. Dekkers

Abstract

Porcine Reproductive and Respiratory Syndrome (PRRS) is a disease of major importance in the swine industry due to its economic impact and its negative effects on animal welfare. PRRS has been estimated to cost the US swine industry alone $664 million per year and impacts all stages of swine production. Current efforts to contain PRRS include biosecurity and vaccination strategies but these have not been widely successful, partly due to large genetic and antigenic variation observed between different PRRS virus (PRRSV) strains. The PRRS Host Genetics Consortium was created with the goal of increasing understanding of the host genetic response to PRRSV infection and evaluating the potential of genetic selection of pigs that are more resistant to PRRS. Approximately 200 commercial crossbred pigs in each of 15 trials were experimentally infected with either the NVSL-97-7895 (NVSL) or KS-2006-78109 (KS06) isolate of PRRSV at approximately 28 days of age. Serum was collected at 0, 4, 7, 11, 14, 21, 28, 35 and 42 days post infection (dpi). Weights were collected at 0 dpi and weekly thereafter. Tonsils and ear samples for genotyping were collected at 42 dpi. Serum viremia and tonsil virus levels were measured using a semi-quantitative PCR assay. The levels of serum PRRSV N protein specific immunoglobulin G was quantified at 42 dpi using fluorescent microsphere immunoassay, and measurements were reported as a sample to positive ratio (S:P). Monophasic or biphasic Wood's curves were fitted to serum viremia records, and the parameters for these curves were used to derive serum curve characteristics for each animal. Additionally, 2nd order Legendre polynomials were fitted to weight measurements. Serum viremia and weight curve fittings allowed daily serum viremia and daily weights to be interpolated to further explore the dynamics of host response to PRRSV infection. The objectives of this dissertation were to: 1) investigate the potential to select for pigs with increased resistance to PRRS that is independent of virus isolate; 2) assess the usefulness of antibody response as an indicator trait of increased PRRS resistance and characterize the relationship of host antibody response with viremia and weight gain; and 3) investigate whether there is a heritable genetic component to tonsil virus levels and identify factors associated with lower tonsil virus levels in order to reduce PRRSV persistence.

NVSL was found to be a more virulent isolate than KS06, but host genetic response to PRRSV influencing peak serum viremia, weight gain, and S:P is expected to be similar during infection with either of these isolates, as evidenced by the estimated strong positive genetic correlations of response to NVSL infection with KS06 infection. A SNP (WUR10000125) that was previously found to be associated with viral load and weight gain under PRRSV infection with the NVSL isolate was found to be associated with viral load and peak viremia in pigs infected with NVSL or KS06; however, there was no observed effect on weight gain in KS06 infected pigs. This suggests the effect of the quantitative trait locus (QTL) marked by WUR may be dependent on the virulence of the PRRSV variant. The relationships between serum viremia and weight gain over the span of three days three-day weight gain changed throughout the course of infection, and were particularly different for pre- and post-peak serum viremia levels. A dynamic relationship was also observed between S:P and serum viremia or three-day weight gain, suggesting that in order to fully explore the relationship between different PRRS response traits, they need to be considered at multiple time points throughout infection. Three QTL, located in the major histocompatibility complex (MHC), were found to be associated with S:P. These QTL were not associated with serum viremia levels or weight gain, suggesting that the genetic correlations of S:P with these traits are due to regions outside of the MHC. Peak viremia, S:P and weight gain during PRRSV infection were identified as traits which have the most potential for successful selection for improved response to PRRSV infection due to high heritability estimates, high genetic correlations with PRRS serum viral load and the ability to measure these traits relatively easily in an industry setting.

Copyright Owner

Andrew Stephen Hess

Language

en

File Format

application/pdf

File Size

249 pages

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