Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Single-cell RNA sequencing of pandemic influenza A virus-infected human airway epithelial cells

ABSTRACT: To characterize the host response to pandemic IAV infection in its natural target cells, we infected primary human airway epithelial cell (hAEC) cultures wild-type pandemic IAV (WT) or a NS1 mutant virus (NS1R38A) with abrogated dsRNA binding capacity at a multiplicity of infection (MOI) of 0.03. We then profiled the transcriptomes of uninfected cells as well as cells harvested 18 hours post-infection (hpi) using single-cell RNA sequencing (scRNA-seq).

INSTRUMENT(S): Illumina HiSeq 3000

ORGANISM(S): Homo sapiens

SUBMITTER: Ronald Dijkman

PROVIDER: E-MTAB-12159 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:E2 exposure significantly decreased peak viral titer in hNECs from female donors. We used microarray analyses to identify global gene expression patterns between E2 and vehicle exposed hNECs from female donors Influenza causes an acute infection characterized by virus replication in respiratory epithelial cells. The severity of influenza and other respiratory diseases changes over the life course and during pregnancy in women, suggesting that sex steroid hormones, such as estrogens, may be involved. Using primary, differentiated human nasal epithelial cell (hNEC) cultures from adult male and female donors, we exposed cultures to the endogenous 17Î²-estradiol (E2) or select estrogen receptor modulators (SERMs), then infected cultures with a seasonal influenza A virus (IAV) to determine whether estrogenic signaling could affect the outcome of IAV infection and whether these effects where sex-dependent. Estradiol, raloxifene, and bisphenol A decreased IAV titers in hNECs from female, but not male, donors. The estrogenic decrease in viral titer was dependent on the genomic estrogen receptor- 2 (ESR2) as neither genomic ESR1 nor non- genomic GPR30 were expressed in hNEC cultures and addition of the genomic ER antagonist ICI 182,780 reversed the antiviral effects of E2. Treatment of hNECs with E2 had no effect on interferon or chemokine secretion, but significantly downregulated cell metabolic processes, including genes that encode for zinc finger proteins, many of which contain estrogen response elements in their promoters. These data provide novel insights into the cellular and molecular mechanisms of how natural and synthetic estrogens impact IAV infection in respiratory epithelial cells derived from humans. Primary human nasal epithelial cells from females were exposed to E2 for 24h prior to infection, then infected with an H3N2 strain of influenza a virus for 2 hours. At 24 and 48h post infection, hNECs were collected in Trizol for RNA extraction and hybridization on Affymetrix Human Gene ST 2.0 microarrays.

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Single-cell RNA sequencing of pandemic influenza A virus-infected human airway epithelial cells

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