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The overall objective of this thesis was to identify the role of host genetics in susceptibility to viral disease in pigs, using experimental infection with porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV). Co-infection with PRRS virus (PRRSV) and porcine circovirus type 2b (PCV2b) was also investigated, since pigs are rarely infected with PRRSV alone. The study reported in the first chapter was designed to investigate the role of host genetics in response to PRRSV-infection in pigs divergently selected for feed efficiency. Contrary to our hypothesis that the more feed efficient pigs would be more susceptible to disease as a correlated response, results showed that the feed efficient pigs were less affected by the PRRS challenge. Subsequent studies were designed to further investigate the role of host genetics in response to PRRSV-infection by estimating the effect of the guanylate binding protein 5 (GBP5) region (the putative causative gene for a major quantitative trait locus for host response to PRRS) on PRRS vaccination response and host response to PRRSV/PCV2b co-infection. Additional objectives were to identify regions other than GBP5 associated with vaccination and co-infection and regions with a significantly different effect on coinfection response, depending on previous vaccination for PRRS. Results from these studies showed that the GBP5 region had a significant effect on PRRS vaccination viral load (VL), PRRS VL, and PCV2b VL (for pigs previously vaccinated against PRRSV). Regions other than GBP5 were not significantly associated with vaccination VL or PRRS VL, but several single nucleotide polymorphisms (SNPs) near the major histocompatibility complex were significantly associated with PCV2b VL. Multiple SNPs were also associated with growth rate following vaccination and co-infection, including

The role of host genetics in susceptibility to viral disease in pigs