Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

RNA-Seq of healthy adult volunteers following experimental infection with Influenza A/Belgium/4217/2015 (H3N2)

ABSTRACT: The uploaded data has been generated from the analysis of nasal scrape samples from two clinical studies registered on ClinicalTrials.gov with identifier ID NCT02755948 and NCT04204993. Primary objectives were to establish the human infection challenge model using a novel H3N2 influenza A virus (IAV, influenza A/Belgium/4217/15) at Imperial College London and to test the hypothesis that influenza lead to quantitative and functional differences in innate and T-cell responses between infected, uninfected, symptomatic and asymptomatic participants. The data is to remain private until the publishing of the relative results.

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Homo sapiens

SUBMITTER: Pete Dayananda

PROVIDER: E-MTAB-13038 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Seasonal influenza outbreaks and recurrent influenza pandemics present major challenges to public health. By studying immunological responses to influenza in different host species, it may be possible to discover common mechanisms of susceptibility in response to various influenza strains. This could lead to novel therapeutic targets with wide clinical application. Using a mouse-adapted strain of influenza (A/HK/1/68-MA20 [H3N2]), we produced a mouse model of severe influenza (p-flu) that reproduces the hallmark high viral load and overexpression of cytokines associated with susceptibility to p-flu in humans. We mapped genetic determinants of the host response using a panel of 29 closely related mouse strains (AcB/BcA panel of recombinant congenic strains) created from influenza-susceptible A/J and influenza-resistant C57BL/6J (B6) mice. Combined clinical quantitative trait loci (cQTL) and lung expression QTL (eQTL) mapping identified candidate genes for two sex-specific QTLs on chromosomes 2 and 17. The former includes the previously described Hc gene, a deficit of which is associated with the susceptibility phenotype in females. The latter includes the phospholipase gene Pla2g7 and Tnfrsf21, a member of the tumor necrosis factor receptor superfamily. Confirmation of the gene underlying the chromosome 17 QTL may reveal new strategies for influenza treatment. To identify eQTLs, we reanalyzed lung expression data previously obtained by Lee et al (2006) on MGU74Av2 microarrays (Affymetrix) for 54 mice (13BcA, 12AcB, B6 and A/J mice in duplicate) using Custom CDFv12 to reorganize oligonucleotide probes based on the latest genome and transcriptome information. We inferred an A/J or B6 strain of origin for each gene based on the genotype of surrounding markers with a call rate of 96.7%. If a gene was in between A/J and B6 markers for a given RCS, it was coded as NA. Expression values were normalized using the Robust Multi-array Analysis (RMA) for Affymetrix gene chips. To define the association between differentially expressed genes and genotypes, ANOVA was conducted on a per-gene basis using the linear model Expression ~ DSO + BG + DSO*BG, where background (BG) and donor strain of origin (DSO) were coded as binary phenotypes corresponding to A/J or B6. The cutoff for genome-wide significance was computed using the BenjaminiM-bM-^@M-^SHochberg correction. For reference, the paper by Lee (2006): http://www.ncbi.nlm.nih.gov/pubmed/16449383

Dataset Information

RNA-Seq of healthy adult volunteers following experimental infection with Influenza A/Belgium/4217/2015 (H3N2)

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