Peste-des-petits-ruminants virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA736161 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14766880_1.fastq.gz | Fastqsanger.gz | |||
| SRR14766880_2.fastq.gz | Fastqsanger.gz | |||
| SRR14766881_1.fastq.gz | Fastqsanger.gz | |||
| SRR14766881_2.fastq.gz | Fastqsanger.gz | |||
| SRR14766882_1.fastq.gz | Fastqsanger.gz |
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Project description:Peste des Petits Ruminants virus N gene partial sequences
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Project description:We report the application of MeRIP-seq (m6A-specific methylated RNA immunoprecipitation) for m6A site profiling of lung tissue under Peste des petits ruminants virus (PPRV) infection.
2022-12-05 | GSE190718 | GEO
Project description:Peste des petits ruminants virus (PPRV) is a negative-stranded RNA virus belonging to the Paramyxoviridae family and causes acute, highly contagious disease in small ruminants. Lysine acetylation plays central role in regulating gene expression. However, the extent and function of lysine acetylation in host cells during PPRV infection remains unknown. In this study, intensive proteomic quantification analysis of the proteome and acetylome of PPRV-infected Vero cells was performed using dimethylation labeling-based quantitative proteomics. As results, we identified 4729 proteins and 1068 acetylated proteins with 2641 quantified modification sites detected by mass spectrometry, of which 304 acetylated proteins with 410 acetylation sites were significantly acetylated in response to PPRV infection. Bioinformatics analyses revealed that the differentially acetylated proteins participated in carbohydrate catabolic and DNA metabolic process, and were associated with multifarious functions, suggesting that intracellular activities were extensively changed after PPRV infection. Protein-protein interaction network of the identified proteins further indicated that a variety of chaperone and ribosome processes were modulated by acetylation. To our knowledge, this is the first study on acetylome in host cell infected with PPRV. It provides an important point for future studies on the acetylated proteins involved in the host response to PPRV replication.
2023-10-24 | PXD025081 | Pride
Project description:Peste des petits ruminants virus (PPRV) belongs to the genus Morbillivirus that causes an acute and highly contagious disease in goats and sheep. Virus infection can trigger the change in the cellular microRNA (miRNA) expression profile, which play important post-transcriptional regulatory roles in gene expression and can greatly influence viral replication and pathogenesis. Here, we employed deep sequencing technology to determine cellular miRNAs expression profile in goat peripheral blood mononuclear cells (PBMCs) infected with Nigeria 75/1 vaccine virus, a widely used vaccine strain for mass vaccination programs against Peste des petits ruminants (PPR). Expression analysis demonstrated that PPRV infection can elicit 316 significantly differentially expressed (DE) miRNAs including 103 known and 213 novel miRNAs candidates in infected PBMCs at 24 hours post-infection as compared with mock control. Target prediction and functional analysis of these DEmiRNAs revealed significant enrichment for several signaling pathways including TLR signaling pathways, PI3K-Akt, endocytosis, viral carcinogenesis, and JAK-STAT signaling pathways. This study provides a valuable basis for further investigation on the roles of miRNAs in PPRV replication and pathogenesis.
2020-08-18 | GSE156378 | GEO
Project description:Contrasting gene expression profiles of monocytes and lymphocytes from Peste-des-petits-ruminants virus infected goats
| PRJNA548075 | ENA
Project description:Peste des Petits Ruminants (PPR) is a highly infectious disease caused by a virus of the genus Morbillivirus (PPRV), infecting mainly sheep and goat. Susceptibility of host can vary widely with host breed and virus strain. The mechanisms underlying this variability are not well understood. Here, we carried out the first comparative in vitro study on goat peripheral blood mononuclear cells (PBMCs) infected with PPRV strains of different virulence, vaccine strain (N75/1), low- (IC89), and high-virulent strain (MA08). Goat PBMCs were infected by the different strains and stimulated with Concanavalin A (Con A), and proteome changes of these cells were evaluated during the infection. The level of PPRV replication was assessed first by RT-qPCR quantification of viral N mRNA and by labelling the viral N protein inside the cells with specific antibodies and analysed by flow cytometry. The dynamics of PBMC sub-populations were also evaluated by flow cytometry. Our results showed that viral replication is critical for PPRV inhibitory effect on PBMCs proliferation. Highly virulent MA08 strain reached a higher level of replication in ConA-stimulated PBMCs and induced higher mortality compared to other strains. Low-virulent IC89 strain showed the lower replication level and cell proliferative inhibitory capacities. Differences in immune genes expression levels were assessed using RNAseq analysis and protein expression was compared using mass spectrometry. Analysis of these data provided the transcriptional and proteome landscape of PBMCs infected with these strains. The possible association between the transcriptional and proteome landscape and changes in immune cell subpopulations dynamics was explored.
2021-11-03 | PXD024890 | Pride
Project description:Peste des petits ruminants virus (PPRV) infection causes highly contagious and severe disease in domestic and wild ruminants. It is widely reported that PRRV infection causes considerable innate immunosuppression in its host and promotes viral replication. However, how does the host rescue the innate immune response to counteract this immunosuppression during viral replication is poorly understood. The goat fetal fibroblasts (GFFs) have been commonly used as host-original cells to investigate the pathogenesis of PPRV. To explore the mechanisms of how host counteracts PPRV-mediated innate immunosuppression, a high-throughput quantitation proteomic approach (iTRAQ in conjunction with LC-MS/MS) was used to investigate the proteome landscape of GFFs in response to PPRV infection. Eventually, the proteomic analysis gained 497 up-regulated proteins and 358 down-regulated proteins (PPRV-infected cells versus mock-infected cells). The complement and coagulation cascades, protein digestion and absorption, and cytokine-cytokine receptor interaction pathways were significantly regulated in response to PPRV infection. ErmineJ analysis of the differentially expressed proteins (DEPs) identified the significantly enriched GO categories for response to interferon-gamma and positive regulation of ERK1 and ERK2 cascade. In addition, many immune related proteins, such as interferon gamma, 2'-5'-oligoadenylate synthase-like protein, toll-like receptor 9, toll-like receptor 6, NOD1, plasminogen activator inhibitor 1, and Wnt-5a were significantly upregulated. This suggested that the innate immune response was triggered during PPRV infection in GFFs. We subsequently identified that the E3 ubiquitin ligase FANCL was critically involved in regulation of the innate immune response during PPRV infection. FANCL inhibited PPRV infection by enhancing type I interferon (IFN) and interferon-stimulated genes (ISGs) expression. Further study indicated that FANCL induced type I IFN production by promoting TBK1 phosphorylation, and therefore impairing PPRV-mediated immunosuppression and revealing an antiviral function against PPRV.
2021-07-26 | PXD022271 | Pride
Project description:Viruses have evolved numerous strategies to impair immunity so that they can replicate more efficiently, such as the immunosuppressive effects of Morbillivirus infection. In the present work we hypothesized that the highly contagious morbillivirus Peste des Petits Ruminants virus (PPRV) could target monocytes and dendritic cells (DC) to contribute to the immunosuppressive effects produced by the infection. Monocytes isolated from healthy sheep donor, a natural host of the disease, could be infected by PPRV and this impaired the differentiation and phagocytic ability of immature monocyte-derived DC (MoDC). Ovine MoDC could be productively infected by PPRV, and this drastically reduced MoDC capacity to activate allogeneic T cell responses. Transcriptomic analysis of infected MoDC indicated that several tolerogenic DC signature genes were upregulated upon PPRV infection.
2022-09-06 | GSE203515 | GEO
Project description:Field-adapted full genome sequencing of peste-des-petits-ruminants virus using Nanopore sequencing
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