PRRSv
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB46770 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR6405400_1.fastq.gz | Fastqsanger.gz | |||
| ERR6405400_2.fastq.gz | Fastqsanger.gz | |||
| ERR6405410_1.fastq.gz | Fastqsanger.gz | |||
| ERR6405410_2.fastq.gz | Fastqsanger.gz | |||
| ERR6405420_1.fastq.gz | Fastqsanger.gz |
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Project description: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.
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