Impact of porcine reproductive and respiratory syndrome virus on muscle metabolism of growing pigs1.

Abstract

Porcine reproductive and respiratory syndrome (PRRS) virus is one of the most economically significant pig pathogens worldwide. However, the metabolic explanation for reductions in tissue accretion observed in growing pigs remains poorly defined. Additionally, PRRS virus challenge is often accompanied by reduced feed intake, making it difficult to discern which effects are virus vs. feed intake driven. To account for this, a pair-fed model was employed to examine the effects of PRRS challenge and nutrient restriction on skeletal muscle and liver metabolism. Forty-eight pigs were randomly selected (13.1 ± 1.97 kg BW) and allotted to 1 of 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 days postinoculation (dpi) 10 and 17, 8 pigs per treatment were euthanized and tissues collected. Tissues were assayed for markers of proteolysis (LM only), protein synthesis (LM only), oxidative stress (LM only), gluconeogenesis (liver), and glycogen concentrations (LM and liver). Growth performance, feed intake, and feed efficiency were all reduced in both PRRS+ and PF pigs compared with Ad pigs (P < 0.001). Furthermore, growth performance and feed efficiency were additionally reduced in PRRS+ pigs compared with PF pigs (P < 0.05). Activity of most markers of LM proteolysis (μ-calpain, 20S proteasome, and caspase 3/7) was not increased (P > 0.10) in PRRS+ pigs compared with Ad pigs, although activity of m-calpain was increased in PRRS+ pigs compared with Ad pigs (P = 0.025) at dpi 17. Muscle reactive oxygen species production was not increased (P > 0.10) in PRRS+ pigs compared with Ad pigs. However, phosphorylation of protein synthesis markers was decreased in PRRS+ pigs compared with both Ad (P < 0.05) and PF (P < 0.05) pigs. Liver gluconeogenesis was not increased as a result of PRRS; however, liver glycogen was decreased (P < 0.01) in PRRS+ pigs compared with Ad and PF pigs at both time points. Taken together, this work demonstrates the differential impact a viral challenge and nutrient restriction have on metabolism of growing pigs. Although markers of skeletal muscle proteolysis showed limited evidence of increase, markers of skeletal muscle synthesis were reduced during PRRS viral challenge. Furthermore, liver glycogenolysis seems to provide PRRS+ pigs with glucose needed to fuel the immune response during viral challenge.