Host transcriptional response to porcine reproductive and respiratory syndrome virus persistent infection

Both virulent and live-attenuated PRRSV strains can establish persistent infection in lymphoid tissues of pigs. To investigate the mechanisms of PRRSV persistence, we performed transcriptional analysis of inguinal lymphoid tissue of pigs experimentally infected with an attenuated PRRSV strain. A total of 6,404 differentially expressed genes (DEGs) were detected of which 3,690 DEGs were upregulated and 2,444 DEGs were downregulated. Specifically, genes involved in innate immune responses and chemokine and receptors associated with T cell homing to lymphoid tissues were down regulated. As a result, homing of virus-specific T cells to lymphoid tissues seems to be ineffective, evidenced by the lower frequencies of virus-specific T cells in lymphoid tissue than in peripheral blood. Genes associated with T cells exhaustion were upregulated. Likewise, genes involved in the anti-apoptotic pathway were upregulated. Collectively, the data suggested that PRRSV establishes a pro-survival microenvironment in lymphoid tissue by suppressing innate immune responses, T cell homing and preventing cell apoptosis. Overall design: For both control (mock) and infected pigs the transcriptome of the lymphoid tissue was sequenced with five biological replicates each.