In vitro study of role of Sigma B in pathogenesis of Avian Reovirus
Ontology highlight
ABSTRACT:
ORGANISM(S): Gallus gallus
PROVIDER: GSE103067 | GEO | 2018/05/09
REPOSITORIES: GEO
Similar Datasets
Project description:Avian reoviruses, members of Orthoreovirus genus was known to cause diseases like tenosynovitis, runting-stunting syndrome in chickens. Among eight structural proteins, the proteins of S-class are mainly associated with viral arthritis but the significance of σB protein in arthritis is not established till date. In this infection pathological condition together with infection of joints often leads to arthritis because joints consists of cartilage which forms lubricating surface between two bones, and has limited metabolic, replicative and repair capacity. To establish the role of σB protein in arthritis, an in-vitro microarray study was conducted consisting four groups viz. virus infected and control; pDsRed-Express-N1-σB and empty pDs-Red transfected, CEF cells. With cut-off value as FC ≥2, p value <0.05, 6709 and 4026 numbers of DEGs in virus and σB, respectively were identified. The Ingenuity Pathway Analysis gave an idea about the involvement of σB protein in "osteoarthritis pathway", which was activated with z-score with 3.151. The pathway "Role of IL-17A in arthritis pathway" was also enriched with -log (p-value) 1.64. Among total 122 genes involved in osteoarthritis pathway, 28 upregulated and 11 downregulated DEGs were common to both virus and σB treated cells. Moreover, 14 upregulated and 7 downregulated were unique in σB transfected cells. Using qRT-PCR for IL-1B, BMP2, SMAD1, SPP1 genes, the microarray data was validated. We concluded that during ARV infection σB protein, if not fully partially leads to molecular alteration of various genes of host orchestrating the different molecular pattern in joints, leading to tenosynovitis syndrome.
| S-EPMC5929409 | biostudies-literature
Project description:We infected DF-1 cells with avian reovirus, and then used high-throughput sequencing to detect changes in miRNA expression profiles. This research provides a more comprehensive understanding of the interaction between viruses and host cells
2022-06-27 | GSE181193 | GEO
Project description:Changes of miRNA expression profile after avian reovirus infection
| PRJNA751037 | ENA
Project description:Avian virus Avian virus YT-2014 Genome sequencing
| PRJNA267235 | ENA
Project description:Mucosal surfaces are common sites of pathogen colonization/entry. Effective mucosal immunity by vaccination should provide protection at this primary infection site. Our aim was to develop a new vaccination strategy that elicits a mucosal immune response. A new strain of Enterococcus faecium, a non pathogenic lactic acid bacteria (LAB) with strong cell adhesion ability, was identified and used as a vaccine vector to deliver two model antigens. Specifically, sigma (?) C protein of avian reovirus (ARV), a functional homolog of mammalian reovirus ?1 protein and responsible for M-cell targeting, was administered together with a subfragment of the spike protein of infectious bronchitis virus (IBV). Next, the effect of immunization route on the immune response was assessed by delivering the antigens via the LAB strain. Intranasal (IN) immunization induced stronger humoral responses than intragastic (IG) immunization. IN immunization produced antigen specific IgA both systemically and in the lungs. A higher IgA titer was induced by the LAB with ARV ?C protein attached. Moreover, the serum of mice immunized with LAB displaying divalent antigens had much stronger immune reactivity against ARV ?C protein compared to IBV-S1. Our results indicate that ARV ?C protein delivered by LAB via the IN route elicits strong mucosal immunity. A needle-free delivery approach is a convenient and cost effective method of vaccine administration, especially for respiratory infections in economic animals. Furthermore, ARV ?C, a strong immunogen of ARV, may be able to serve as an immunoenhancer for other vaccines, especially avian vaccines.
| S-EPMC7115360 | biostudies-literature
Project description:Background：Dendritic cells (DCs), have the most important antigen presenting ability and played an irreplaceable role in recognizing and clearing virus. Antiviral responses must rapidly defend against infection while minimizing inflammatory damage, but the mechanisms that regulate the magnitude of response within an infected cell are not well understood. MicroRNA, small non-coding RNAs, that can regulate dendritic cells to inhibit the infection and replication of avian influenza virus. Here, we global analyses how avian DCs response to H9N2 avian influenza virus (AIV) and provide a potential mechanism of how avian microRNA defending H9N2 AIV replication. Results： Here, we global analyses how avian DCs response to H9N2 avian influenza virus (AIV) and provide a potential mechanism of how avian microRNA defending H9N2 AIV replication. First, we found that both active and inactive H9N2 AIV enhance the ability of DCs to present antigens and activate T lymphocytes. Next, total microarray analyses suggested that H9N2 AIV stimulation involved in protein localization, nucleotide binding and leukocyte transendothelial migration and MAPK signal pathways. Moreover, we construct 551 transcription factor (TF)-microRNA-mRNA loops based on the above analyses. Furthermore, we found that HA fragment could not activate DCs, while truncated HA highly increased the immune function of DCs by activating ERK and STAT3 signal pathway. Last, our insight research not only gained that gga-miR1644 might target to MBNL2 to enhanced avian DCs in inhibiting virus replication, but also suggested that gga-miR6675 target to the NLS of PB1 to trigger the silencing of PB1 genes and lead to inhibition of H9N2 avian influenza viral replication. All together, our innovative research will shed new light on the roles of avian microRNA in evoking avian DCs and inhibiting virus replication, which will suggest new strategies to combat avian influenza virus.
2017-07-08 | GSE100916 | GEO