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Distinctive cellular and metabolic reprogramming in porcine lung myeloid cells infected with type I PRRSV strains

ABSTRACT: Distinctive cellular and metabolic reprogramming in porcine lung myeloid cells infected with type I PRRSV strains

PROVIDER: PRJNA615854 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11433900.fastq.gz	Fastqsanger.gz
	SRR11434000.fastq.gz	Fastqsanger.gz
	SRR11434100.fastq.gz	Fastqsanger.gz
	SRR11434200.fastq.gz	Fastqsanger.gz
	SRR11434300.fastq.gz	Fastqsanger.gz

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Distinctive cellular and metabolic reprogramming in porcine lung myeloid cells infected with type I PRRSV strains

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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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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Distinctive Cellular and Metabolic Reprogramming in Porcine Lung Mononuclear Phagocytes Infected With Type 1 PRRSV Strains.

Project description:Porcine reproductive and respiratory syndrome (PRRS) has an extensive impact on pig production. The causative virus (PRRSV) is divided into 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 phagocyte (MNP) subtypes, including conventional dendritic cells types 1 (cDC1) and 2 (cDC2), monocyte-derived DCs (moDC), and pulmonary intravascular macrophages (PIM), have not been thoroughly investigated. Here, we analyze 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, and in vitro infection with Lena confirmed the higher ability of this strain to modulate host response. Machine learning (ML) and gene set enrichment analysis (GSEA) unraveled additional relevant genes and pathways modulated by FL13 infection that were not identified by conventional analyses. GSEA increased the cellular pathways enriched in the FL13 data set, but ML allowed a more complete comprehension of functional profiles during FL13 in vitro infection. Data indicates that cellular reprogramming differs upon Lena and FL13 infection and that the latter might keep antiviral and inflammatory macrophage/DC functions silent. Although the slow replication kinetics of FL13 likely contribute to differences in cellular gene expression, the data suggest distinct mechanisms of interaction of the two viruses with the innate immune system during early infection.

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Project description:Porcine reproductive and respiratory syndrome virus (PRRSV) is a causative agent of an important infectious disease causing serious economic losses to swine industry called PRRS (porcine reproductive and respiratory syndrome). The clinical signs of this syndrome indcude respiratory disorders, abortions and variable mortality in piglets. To compare the virulence of highly diverse East European strains belonging to subtype 2 (Russian strain ILI and Belarusian strain BOR) and Danish strain from classical subtype 1 (DAN) the experimental study enrolling infection of piglets was performed. Gene expression profiles of peripheral blood mononuclear cells (PBMC) of piglets infected with three PRRSV strains vs control piglets were analysed by microarray analysis to gain insight into transcriptome changes after PRRSV infection.

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