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Type I PRRSV transcriptome

ABSTRACT: Direct RNA-seq of Type I PRRSV isolated from pig tissues

PROVIDER: PRJEB16756 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1769903_1.fastq.gz	Fastqsanger.gz
	ERR1769903_2.fastq.gz	Fastqsanger.gz
	ERR1769904_1.fastq.gz	Fastqsanger.gz
	ERR1769904_2.fastq.gz	Fastqsanger.gz
	ERR1769905_1.fastq.gz	Fastqsanger.gz

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PRRSV counteracts type I interferon-induced antiviral state

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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Project description:Porcine reproductive and respiratory syndrome (PRRSV) is a devastating pathogen for the pig industry worldwide. PRRSV mainly infects porcine alveolar macrophage (PAM). In the present study, single-cell RNA sequencing (scRNA-seq) was employed to characterize the host transcriptome responses of PAMs infected with a virulent PRRSV strain in vivo and ex vivo. Increase ofpro-inflammatory and anti-apoptotic genes was correlated with the increase of infection (expression of the virus ORF7 transcript).

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Project description:The Porcine Reproductive and Respiratory Syndrome (PRRS) has an extensive impact on pig production. The causative virus (PRRSV) is divided in two species, PRRSV-1 (European origin) and PRRSV-2 (North American origin). Within PRRSV-1, PRRSV-1.3 strains such as Lena are more pathogenic than PRRSV-1.1 strains such as Flanders 13 (FL13). To date, the molecular interactions of PRRSV with primary lung mononuclear phagocytes (MNP) subtypes including conventional dendritic cells type 1 (cDC1) and type 2 (cDC2), monocyte-derived DCs (moDC) and parenchymal macrophages (PIM) have not been thoroughly investigated. Here, we analysed the transcriptome profiles of in vivo FL13-infected parenchymal MNP subpopulations and of in vitro FL13- and Lena-infected parenchymal MNP. The cell specific expression profiles of in vivo sorted cells correlated with their murine counterparts (AM, cDC1, cDC2, moDC) with the exception of PIM. Both in vivo and in vitro, FL13 infection altered the expression of a low number of host genes while in vitro infection with Lena confirmed the higher ability of this strain to modulate host response. Machine learning (ML) and GSEA analyses unraveled additional relevant genes and pathways modulated by FL13 infection that were not identified by conventional analyses. GSEA increased the cellular pathways enriched in FL13 dataset, but ML allowed a more complete comprehension of functional profiles during FL13 in vitro infection. Data indicated that cellular reprogramming differed upon Lena and FL13 infection, and that the latter keeps antiviral and inflammatory macrophages/DC functions silent, suggesting a different mechanism of pathogenesis during early infection.

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Genetic variation contribute to different susceptibility to HP-PRRSV infection across pig breeds

Project description:Purpose: To characterize the differential mRNA expression profiles of lung tissues upon PRRSV infection in different pig breeds, using NGS techonology, we sequenced mRNAs of the lungs of Tongcheng and Landrace pigs before (0 dpi) and after (3, 5, 7 dpi) infection with high-pathogenic PRRSV (HP-PRRSV). Methods: The mRNA expression profiles of the lungs of Tongcheng and Landrace pigs before (0 dpi) and after (3, 5, 7 dpi) HP-PRRSV infection were produced by using solexa platform. The raw reads with low qualities were filtered and the clean high quality reads were mapped to Ensembl Sus reference genome 10.2.71 using BOWTIE2. The unique mapped reads were retained for mRNA expression analysis. The raw reads counts of each mRNA were calculated by HTseq and the differentially expressed mRNA (Fold change >2; FDR <0.05) were called using DEGseq.

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PRRSv

Project description:PRRSv resequencing project

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