Ontology highlight
ABSTRACT:
PROVIDER: PRJNA730044 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14552500.fastq.gz | Fastqsanger.gz | |||
| SRR14552501.fastq.gz | Fastqsanger.gz | |||
| SRR14552502.fastq.gz | Fastqsanger.gz | |||
| SRR14552503.fastq.gz | Fastqsanger.gz | |||
| SRR14552504.fastq.gz | Fastqsanger.gz |
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Project description:Swine coronavirus-porcine epidemic diarrhea virus (PEDV) with specific susceptibility to pigs has existed for decades, and recurrent epidemics caused by mutant strains have swept the world again since 2010. Here, single-cell RNA-sequencing was used to perform a systematic analysis of pig small intestines infected with PEDV for the first time. Multiple cell types were identified by representative markers, including the unique marker DNAH11 of tuft cells. Meanwhile, the goblet and tuft cells were also susceptible to PEDV except enterocytes. PEDV infection obviously upregulated REG3G, which significantly inhibited virus replication. Notably, IFN-DELTAs in goblet and enterocyte progenitor cells were increased in virus infected piglet, and IFN-DELTA5 could induce GBP1, ISG15, OAS2 and IFITM1 dramatically raised in IPEC-J2 cells and restricted PEDV replication. Complement molecules were mainly expressed in intestinal cells excepting tuft cells, but PEDV decreased C3, C4A, and C5 in enterocytes, thus escaping the antiviral effect of C3. Finally, enterocytes expressed almost all coronavirus entry factors, and PEDV infection caused significant upregulation of the coronavirus receptor ACE2 in porcine enterocyte cells. In summary, this study systematically studied the response of different cell types in small intestine of pigs after PEDV infection, which deepened the understanding of viral pathogenesis.
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Project description:Transcriptome sequencing of IPEC-J2 cells infected with PEDV
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Project description:Transcriptome modulation analysis of cytomegalovirus-infected immature monocyte-derived dendritic cells
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Project description:Porcine epidemic diarrhea virus (PEDV) causes severe intestinal damage and high mortality in neonatal piglets. The continuous emergence of new strains has brought new challenges to prevention and control. In this study, we isolated and characterized a prevalent PEDV virulent strain, and analyzed 19,612 jejunal cells from PEDV-infected and control piglets using single-cell sequencing, revealing significant changes in cellular composition, gene expression, and intercellular communication. In response to PEDV infection, epithelial repair was enhanced through increased proliferation and differentiation of stem cells, transit-amplifying (TA) cells, and intestinal progenitor cells into enterocytes. Additionally, PEDV disrupted intercellular communication, compromising epithelial functionality while triggering immune responses, with IFN-II and IL-10 signaling activation acting as critical regulators of immune balance and tissue homeostasis. Beyond enterocytes, viral genes were detected in various other cell types. Further experiments confirmed that PEDV could initiate replication in B and T lymphocytes but was unable to produce infectious progeny, with T cells additionally undergoing virus-induced apoptosis. These findings provide new insights into PEDV tropism, immune evasion, and epithelial repair, revealing complex host-pathogen interactions that shape disease progression and tissue regeneration, thereby contributing to a better understanding of enteric coronavirus pathogenesis.
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Project description:The global transcriptome of whole lungs extracted from M. tuberculosis infected C57BL6 mice
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Project description:The immune system is thought to be fragile in the neonate, which is susceptible to pathogens. Exosomes are a type of vehicles existing in the body fluid and participate in many biological processes, especially the immune response. Inorder to investigate the roles that exosomes may play during virus infection in the neonate, porcine epidemic diarrhea virus (PEDV), a devastating enteric virus to newborn piglets, was selected for infection. Serum exosomes were then isolated from the newborn-piglets infected or mock-infected with PEDV and followed by a label-free LC-MS/MS based comparative quantitative proteomic analysis. Among 441 proteins detected in the serum exosomes, there were lots of complement proteins. The expression level of the complement C3, C6 and CFB suffered drastic changes due to PEDV infection. After the confirmation by western-blot assay, we then investigated the function of these exosomes on PEDV infection and discovered that the exosomes from mock-infected newborn piglets restricted PEDV infection but this inhibition disappeared after exosomes were heat-inactivated, suggesting that the complement is one of the key antiviral molecules. These findings will facilitate the understanding of the antiviral response of the neonate mediated by exosomes
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Project description:Deoxynivalenol (DON) frequently detected in a wide range of foods and feeds, inducing cytotoxicity to animals and humans. N6-methyladenosine (m6A) is an important epitranscriptomic marker with high abundance in eukaryotic mammals mRNAs. However, the role of the m6A methylomes in DON damage is still poorly understood. Here, we investigated the m6A transcriptome-wide profile in intestinal porcine epithelial cells (IPEC-J2) with and without 1000 ng/mL DON treatment via m6A sequencing and RNA sequencing. In total, 5406 new m6A peaks appeared with the disappearance of 2615 peaks in DON-induced IPEC-J2. The unique m6A-modified genes in DON-induced IPEC-J2 were associated with TNF signaling pathway. We identified 733 differentially expressed mRNA transcripts with hyper-methylated or hypo-methylated m6A peaks between DON-induced IPEC-J2 and normal IPEC-J2. Protein interaction network analysis and qPCR validation suggested that CSF2 probably acts as a promising new target for combating DON damage in IPEC-J2. Our first report of m6A transcriptome-wide map of IPEC-J2 cells presented here provides a starting roadmap for uncovering m6A functions that may affect DON infection.
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Project description:Porcine epidemic diarrhea virus (PEDV) has reemerged as the main pathogen of piglets due to its high mutation feature. Monolaurin (ML) is a natural compound with a wide range of antibacterial and antiviral activities. However, the role of ML in PEDV infection is still unknown. This study aimed to evaluate the effect of ML on the growth performance, intestinal function, virus replication and cytokine response in piglets infected with PEDV, and to reveal the mechanism through proteomics analysis. Piglets were orally administrated with ML at a dose of 100 mg/kg·BW for 7 days before PEDV infection. Results showed that although there was no significant effect on the growth performance of piglets, ML administration alleviated the diarrhea caused by PEDV infection. ML administration promoted the recovery of intestinal villi, thereby improving intestinal function. Meanwhile, PEDV replication was significantly inhibited, and PEDV-induced expression of IL-6 and IL-8 were decreased with ML administration. Proteomics analyses showed that 38 proteins were differentially expressed between PEDV and ML+PEDV groups, and were significantly enriched in the interferon-related pathways. This suggests ML could promote the restoration of homeostasis by regulating the interferon pathway. Overall, the present study demonstrated ML could confer a protective effect against PEDV infection in piglets, and may be developed as a drug or feed additive to prevent and control PEDV disease.
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