374 Metabolic response of pigs to Porcine Reproductive and Respiratory Syndrome virus infection and nutrient restriction

Porcine reproductive and respiratory syndrome (PRRS) virus is one of the most economically significant pig pathogens worldwide. The virus infects pigs at all production stages and significantly reduces the tissue accretion of growing pigs. However, the metabolic explanation for these reductions in tissue accretion remain poorly defined. Additionally, PRRS virus infection is often accompanied by reductions in feed intake, making it difficult to discern which effects are virus versus feed intake driven. To account for this, a pair-fed model was employed to examine the effects of PRRS infection and nutrient restriction on skeletal muscle and liver metabolism. Forty-eight pigs were randomly selected (11.34 ± 1.54 kg BW) and allotted to 3 treatments (n = 16 pigs/treatment): 1) PRRS naïve, ad libitum fed (Ad), 2) PRRS-inoculated, ad libitum fed (PRRS+), and 3) PRRS naïve, pair-fed to the PRRS-inoculated pigs’ daily feed intake (PF). At dpi 10 and dpi 17, 8 pigs per treatment were euthanized and tissues collected. Tissues were assayed for markers of proteolysis [longissimus skeletal muscle (LM) only], oxidative stress (LM only), and glycogen levels (LM and liver). Markers of LM proteolysis (calpain, 20s proteasome, caspase 3/7 activities) and mitochondrial reactive oxygen species production did not differ (P > 0.10) between treatment groups at either timepoint. Liver glycogen stores were reduced (P < 0.001) in PRRS+ pigs compared with both Ad and PF pigs, which did not differ from each other. Muscle glycogen did not differ (P > 0.10) between treatment groups. However, liver glycogen stores were completely depleted due to PRRS+, but not pair-feeding, indicating that liver glycogen stores and glucose are preferentially utilized by pigs to produce and support immune components. These data suggest that even under severe viral challenge and feed restriction, the pig does not upregulate LM proteolysis to re-allocate nutrients to fuel the immune response.