PRRSV counteracts type I interferon-induced antiviral state

ABSTRACT: Porcine reproductive and respiratory syndrome (PRRS) is an economically important disease with a significant impact on the pig industry. It is caused by PRRS virus (PRRSV), which predominantly infects and replicates in porcine pulmonary alveolar macrophages (PAMs), providing a useful in vitro model for understanding the host immune response to PRRSV infection. We pretreated PAMs with porcine IFN-α to induce an antiviral state within the cells and subsequently infected them with highly pathogenic (HP)-PRRSV. Changes in global gene expression in IFN-α-pretreated PAMs in response to HP-PRRSV infection were determined by RNA-sequence analysis. A total of 346 differentially expressed genes (DEGs) were transcriptionally upregulated by porcine IFN-α. Among these up-regulated DEGs, 93 showed significantly attenuated expression levels in response to HP-PRRSV infection. These attenuated DEGs were remarkably enriched in immune-response-related terms, such as 'RIG-Ilike receptor signaling pathway', 'Response to virus', and 'Response to stimulus'. Notably, expression levels of 93.8% (15/16) of antiviral genes (such as PKR, OAS1, IFIT1(ISG56) and ISG15), and genes encoding retinoic-acid-inducible gene-I protein (LOC100737466(DDX58), a cytoplasmic viral RNA sensor), interferon regulatory factor 7 (IRF7, a key transcriptional regulator of type I IFN-dependent immune response), signal transducer and activator of transcription 1 (LOC100738308(STAT1), a transcription factor for IFN-stimulated genes), and tumor necrosis factor-related apoptosis-inducing ligand (TNFSF10, a cytokine initiating proapoptotic signaling cascades) were significantly attenuated by HP-PRRSV infection. These results suggest that HP-PRRSV can counteract the type I IFN-induced antiviral state by interfering with the expression of genes involved in the host-defense response.

ORGANISM(S): Sus scrofa

PROVIDER: GSE77376 | GEO | 2017/01/28

SECONDARY ACCESSION(S): PRJNA310184

REPOSITORIES: GEO