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Non-lytic clearance of influenza B virus from infected cells [scRNA-seq]

ABSTRACT: Influenza B virus (IBV) is an acute respiratory pathogen that induces phenotypic alterations to the lung epithelium, such as the denudation of the respiratory cilium, during and after IBV infection. It has been assumed that these epithelial changes are non-adaptive, and simply the result of cellular death following lytic virus infection. However, previous reports have shown that not all infected cells are killed after viral infection; some cells can completely clear viral RNA and protein and persist in the host long-term. In this study, we utilized a novel recombinant virus in combination with a Cre recombinase-responsive transgenic mouse model to demonstrate that IBV infection leads to the formation of a population of survivor ciliated cells in the proximal airways of infected mice. To ensure that we were studying ciliated cells with markers that were maintained during viral infection in vivo, we performed single-cell transcriptional profiling on infected and surviving ciliated cell populations. We digested mouse lungs and sorted cells using tdTomato as a marker of infection. We sorted cell populations from the lungs of animals mock infected with PBS (Mock) and during active infection (2 DPI). The resulting data revealed that the marker CD24 is consistently expressed on ciliated cells before and during viral infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE116031 | GEO | 2018/12/05

REPOSITORIES: GEO

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Project description:Background: Avian infectious bronchitis virus (IBV) was an major respiratory disease-causing agents that lead to significant losses in birds. Dendritic cells (DCs), an major antigen-presenting cells, influence viruses pathogenicity as well as host immune response. Expression of host non-coding mRNA changes markedly during infectious bronchitis virus (IBV) infection of avian, but their role in regulating host immune function to defend IBV infection has not been explored. Here, microarray, including mRNAs, miRNAs and lncRNAs, were analysed to better understand the interaction between IBV and avian DCs. Results: Firstly, we found that IBV infection can effectively induce avian DCs to become mature. Interestingly, inactivated IBV possess high ability in inducing DC maturation and activating lymphocytes than that in actived IBV stimulated group. Then, result identified that IBV infection induced 1093 upregulated and 845 downregulated mRNAs in avian DCs. Analysis of Gene Ontology suggested that celluar macromolecule and protein location (GO-BP), as well as transcription factor binding (GO-MF) were abundance in IBV infected group. Whilst, pathway analyses suggested that oxidative phosphorylation and T cell receptor signalling pathways might activated in IBV group. Moreover, microRNA (miRNA) and long non-coding RNA (lncRNA) alterations in IBV-stimulated avian DCs were observed. A total of 19 significantly altered (7 up and 12 down) miRNAs and 101 (75 up and 26 down) lncRNAs were identified in IBV-stimulated DCs. Furtherly insight analyses not only gain that regulation of actin cytoskeleton and MAPK signal pathway were contributed to IBV stimulated miRNAs target genes, but also build an regulatory networks based on co-expressed lncRNA and mRNA. Finally, our study identified 2 TF-miRNA (CEBPA-miR1772 and CEBPA-miR21), which we based on to constructed 53 transcription factor (TF)–miRNA–mRNA interactions involving 1 TF, 2 miRNAs, and 53 mRNAs in IBV-stimulated avian DCs.

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Non-lytic clearance of influenza B virus from infected cells [scRNA-seq]

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