Infection with Porcine Reproductive and Respiratory Syndrome virus (PRRSv) impacts immune cell metabolism without evidence of cell-mediated immune response.

Abstract

Abstract Specific metabolic pathways affect immune cell differentiation and function, and the metabolic state of leukocytes may provide a signature associated with a particular condition or treatment. Health challenge in food production animals may warrant dietary changes to meet metabolic demand of the immune system. Porcine reproductive and respiratory syndrome virus (PRRSV) infection negatively impacts pig performance, and the PRRSV-specific immune response is inefficient at providing protection. Given the poor cell-mediated response induced by infection, we hypothesized that the metabolic profile of peripheral blood mononuclear cells (PBMC) from PRRSV-infected pigs would not show a shift to glycolysis, which is a hallmark of T effector cells. Using an Extracellular Flux Analyzer (Seahorse Biosciences) we interrogated the glycolytic and mitochondrial function of PBMC following infection of pigs with PRRSV, and PRRSV-specific cell-mediated immunity. Basal glycolysis of PBMC was not significantly impacted by PRRSV infection, but contrary to our hypothesis, glycolytic capacity and reserve were significantly increased in PBMC from PRRSV-infected pigs over non-infected pigs. The effect of PRRSV infection on PBMC mitochondrial respiration was minimal, with a slight increase in spare respiratory capacity detected. Despite the increased glycolytic capacity of PBMC, there was not a detectable PRRSV-specific cell-mediated immune response. Thus, while there was metabolic signature of lymphocyte activation, it was not associated with a functional response.