Influenza A virus strain:A/Panama/2007/1999
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA598865 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10827546_1.fastq.gz | Fastqsanger.gz | |||
| SRR10827546_2.fastq.gz | Fastqsanger.gz | |||
| SRR10827547_1.fastq.gz | Fastqsanger.gz | |||
| SRR10827547_2.fastq.gz | Fastqsanger.gz | |||
| SRR10827548_1.fastq.gz | Fastqsanger.gz |
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Project description:A novel avian-origin H7N9 influenza A virus (IAV) emerged in China in early 2013 causing mild to lethal human respiratory infections. H7N9 originated from multiple reassortment events between avian viruses and carries genetic markers of human adaptation. Determining whether H7N9 induces a host-response closer to human or avian IAV is important to better characterize this emerging virus. Here we compared the human lung epithelial cell response to infection with A/Anhui/01/13 (H7N9) or highly pathogenic avian-origin H5N1, H7N7, or human seasonal H3N2 IAV. Here, polarized confluent monolayers of Calu-3 cells were infected apically with the avian-origin IAVs A/Anhui/01/2013 (H7N9) [Anhui01], A/Netherland/219/2003 (H7N7) [NL219], A/Vietnam/1203/2004 (H5N1) [VN1203], or a human seasonal virus A/Panama/2007/1999 (H3N2) [Pan99] at an MOI of 1. Time-matched mocks were also included using the same cell stock as the rest of the samples. Culture medium (same as what the virus stock is in) was used for the mock infections. Quadruplicate wells were infected for each virus/timepoint. Measured timepoints were 3, 7, 12 and 24 hours post-inoculation and the RNA was used for transcriptional analysis via microarray.
2014-01-16 | E-GEOD-49840 | biostudies-arrayexpress
Project description:Genome-wide gene expression patterns were measured in human monocyte-derived dendritic cells (DCs) infected in vitro with seasonal H1N1 influenza A/New Caledonia/20/1999. To provide a mechanistic explanation for the timing of gene expression changes over the first 12 hours post-infection, we developed a statistically rigorous enrichment approach integrating genome-wide expression kinetics and time-dependent promoter analysis. Our approach, TI me-Dependent Activity Linker (TIDAL), generates a regulatory network that connects transcription factors associated with each temporal phase of the response into a coherent linked cascade. TIDAL infers 12 transcription factors and 32 regulatory connections that drive the antiviral response to influenza. To demonstrate the generality of this approach, TIDAL was also used to generate a network for the DC response to measles infection. Monocyte-derived DCs were obtained from healthy human blood donors following a standard protocol. The recent seasonal H1N1 influenza virus A/New Caledonia/20/1999 (NC) virus was titrated by immunofluorescence 18 hours after infection of MDCK cell plates using monoclonal antibodies specific for Influenza-NP protein generated by the Mount Sinai Hybridoma Core Facility followed by addition of anti-mouse IgG-FITC and visualization using fluorescent microscopy. For infection of naive DCs, NC stocks were appropriately diluted in DulbeccoM-bM-^@M-^Ys Modified Eagle Medium (DMEM) and added directly into pelleted DCs at a multiplicity of infection (MOI) of 1 After incubation for 40 minutes at 37 M-bM-^WM-&C, fresh DC growth medium (without GMCSF and IL-4) was added back to the infected cells (1 106 cells/ml) for the remainder of the infection. The reaction was stopped at 1, 2, 4, 6, 8, 10, and 12 hours after infection by fixing the cells with RNAprotect Cell Reagent (Qiagen, Duesseldorf Germany). Naive non-infected DCs underwent the same experimental procedure as infected DCs in the absence of virus to ensure that mechanical manipulations could not be responsible for differences in experimental readouts. All time points and controls were performed in triplicates. Cells were homogenized by using QIAshredder microcentrifuge spin-columns (Qiagen, Duesseldorf Germany) and RNA was isolated from cells using Qiagen Micro RNeasy plus kit following the manufactures protocol (Qiagen, Duesseldorf Germany). RNA quality was assayed by determination of the RNA integrity number using the 2100 Bioanalyzer (Agilent). RNA samples were processed and hybridized to HumanHT-12 v4 Expression BeadChip Kit (Illumina San Diego, CA) by the Mount Sinai Genomics Institute following the manufacturerM-bM-^@M-^Ys instructions, and raw expression data were output by the Illumina GenomeStudio software.
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Project description:Determining the role of interferons in the host defence against influenza A virus Methods: Tumor-free human lung explants were obtained from patients undergoing lung surgery at the University Hospital Muenster on the day of surgery. Tissue blocks were individually placed in a 12-well plate in RPMI medium. Virus infection of human lung tissue was performed with seasonal IV H3N2 strain A/Panama/2007/1999. RNA was prepared from tissue homogenates. Results: RNA sequencing revealed significant transcriptional upregulation of genes encoding IFN-α subtypes α1, α2, α8, α14 and α17, which we identified to possess only low to intermediate antiviral activity. In contrast, our experiments provide evidence that subtypes α16, α5 and α4 suppress H3N2 replication 40 – 231 fold more efficiently compared to clinically approved IFN-α2. We detected significantly higher induction of IV restriction factors MxA, RIG-I, OAS1 and PKR by these subtypes compared to the non-active IFN-α1 but correlation of antiviral activity with the expression levels of these restriction factors was not observed. Conclusions: Our results show that IFN-α subtypes differ in their ability to repress H3N2 replication in human lung tissue and emphasize that IFN-α subtypes α16, α5 and α4 have high therapeutic potential and should be further investigated for the prevention and treatment of severe infections with seasonal H3N2.
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