Upper respiratory microbiome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA726994 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16356813_1.fastq.gz | Fastqsanger.gz | |||
| SRR16356813_2.fastq.gz | Fastqsanger.gz | |||
| SRR16356814_1.fastq.gz | Fastqsanger.gz | |||
| SRR16356814_2.fastq.gz | Fastqsanger.gz | |||
| SRR16356815_1.fastq.gz | Fastqsanger.gz |
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Project description:Upper respiratory microbiome Metagenome during SARS-CoV-2 infection
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Project description:Upper respiratory microbiome during SARS-CoV-2
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Project description:The Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has had devastating impacts on our global society. Although vaccines and monoclonal antibody countermeasures have reduced the morbidity and mortality associated with SARS-CoV-2 infection, variants with constellations of mutations in the spike gene threaten their efficacy. Therefore, antiviral interventions that are resistant to further virus evolution may be needed. Here, we show IFN-λ protects against SARS-CoV-2 B.1.351 (Beta) and B.1.1529 (Omicron) variants in three strains of conventional and human ACE2 transgenic mice. Prophylaxis or therapy with nasally-delivered IFN-λ2 limited infection of historical or variant (B.1.351 and B.1.1.529) SARS-CoV-2 strains in both the upper and lower respiratory tracts without causing excessive inflammation. In the lung, IFN-λ was produced preferentially in epithelial cells and acted on radio-resistant cells to protect against of SARS-CoV-2 infection. Thus, inhaled IFN-λ may have promise as a treatment for evolving SARS-CoV-2 variants that develop resistance to antibody-based countermeasures.
2022-02-08 | GSE193990 | GEO
Project description:Unlike other respiratory viruses, SARS-CoV-2 disproportionately causes severe disease in older adults and only rarely in children. To investigate whether differences in the upper airway immune response could contribute to this disparity, we compared nasopharyngeal gene expression in 83 children (<19-years-old; 38 with SARS-CoV-2, 11 with other respiratory viruses, 34 with no virus) and 154 adults (>40-years-old; 45 with SARS-CoV-2, 28 with other respiratory viruses, 81 with no virus). Expression of interferon-stimulated genes (ISGs) was robustly activated in both children and adults with SARS-CoV-2 compared to the respective non-viral groups, with only relatively subtle distinctions. Children, however, demonstrated markedly greater upregulation of pathways related to B cell and T cell activation and proinflammatory cytokine signaling, including TNF, IFNγ, IL-2 and IL-4 production. Cell type deconvolution confirmed greater recruitment of B cells, and to a lesser degree macrophages, to the upper airway of children. Only children exhibited a decrease in proportions of ciliated cells, the primary target for SARS-CoV-2, upon infection with the virus. These findings demonstrate that children elicit a more robust innate and adaptive immune response to SARS-CoV-2 infection in the upper airway that likely contributes to their protection from severe disease in the lower airway.
2021-07-19 | GSE179277 | GEO
Project description:Understanding the pathology of COVID-19 is a global research priority. Early evidence suggests that the microbiome may be playing a role in disease progression, yet current studies report contradictory results. Here, we examine potential confounders in COVID-19 microbiome studies by analyzing the upper respiratory tract microbiome in well-phenotyped COVID-19 patients and controls combining microbiome sequencing, viral load determination, and immunoprofiling. We found that time in the intensive care unit and the type of oxygen support explained the most variation within the upper respiratory tract microbiome, dwarfing (non-significant) effects from viral load, disease severity, and immune status. Specifically, mechanical ventilation was linked to altered community structure, lower species- and higher strain-level diversity, and significant shifts in oral taxa previously associated with COVID-19.
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Project description:Full understanding of the pathophysiology of COVID-19 is critical for adequate treatment and development of vaccine and therapeutics. Although Golden hamster has been emerged as animal model of COVID-19, it is unknown how SARS-CoV-2 enters and infects targeted epithelial cells at molecular and cellular levels. Here, by applying single cell RNA sequencing in the upper respiratory tract, lung, kidney and intestine of golden hamster, we show that the expression profiles of host factors for SARS-CoV-2 infection in specific cell types are similar to that of human. These data can be applied to a larger investigation (data not provided here) into the expression patterns of host cell entry factors of SARS-CoV-2 in golden hamster organs.
2021-01-01 | GSE154564 | GEO
Project description:During the COVID-19 pandemic, three variants of concern (VOC) of the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) emerged globally with increasingly greater ability to evade the immune response and enhanced transmissibility. A critical question we have faced with each new VOC is how well the vaccine based on the ancestral strain will protect. Given vaccine hesitancy, it is also important to address how prior live infections may protect against new variants. To address this later question, K18-hACE2 mice were infected with a low, partially lethal dose of WA1/2020 (WA1), the prototype strain on which the mRNA vaccines are based. On 24 days post-infection (dpi), surviving mice were challenged with WA1, Alpha or Delta. Nasal turbinates and lungs showed active replication on 1- and 3-days post-challenge (dpc) in Alpha- and Delta-, but not WA1- challenge groups. The rate of recovery of Alpha- and Delta-challenged mice lagged behind WA1 with mice showing weight loss despite a greatly dampened proinflammatory response in the lung. In contrast, nasal turbinates had a heightened proinflammatory response for Alpha- and Delta- but not WA1-challenged groups. Inflammatory responses were limited to the upper respiratory tract. Despite this, we did not observe significant difference among the groups in fold change in the neutralizing titer. In summary, infection with a low dose of SARS-CoV-2 confers protection from challenge, but mice in the heterologous challenge group differed in having greater weight loss, viral replication, and a heightened proinflammatory response in the upper respiratory tract.
2023-03-01 | GSE216048 | GEO
Project description:Severe acute respiratory syndrome virus (SARS-CoV) that lacks the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo [1,2]. To identify factors that contribute to rSARS-CoV-ΔE attenuation, gene expression in cells infected by SARS-CoV with or without E gene was compared. Twenty-five stress response genes were preferentially upregulated during infection in the absence of the E gene. In addition, genes involved in signal transduction, transcription, cell metabolism, immunoregulation, inflammation, apoptosis and cell cycle and differentiation were differentially regulated in cells infected with rSARS-CoV with or without the E gene. Administration of E protein in trans reduced the stress response in cells infected with rSARS-CoV-ΔE, with respiratory syncytial virus, or treated with drugs, such as tunicamycin and thapsigarcin that elicit cell stress by different mechanisms. In addition, SARS-CoV E protein down-regulated the signaling pathway inositol-requiring enzyme 1 (IRE-1) of the unfolded protein response, but not the PKR-like ER kinase (PERK) or activating transcription factor 6 (ATF-6) pathways, and reduced cell apoptosis. Overall, the activation of the IRE-1 pathway was not able to restore cell homeostasis, and apoptosis was induced probably as a meassure to protect the host by limiting virus production and dissemination. The expression of proinflammatory cytokines was reduced in rSARS-CoV-ΔE-infected cells compared to rSARS-CoV-infected cells, suggesting that the increase in stress responses and the reduction of inflammation in the absence of the E gene contributed to the attenuation of rSARS-CoV-ΔE. We used Affymetrix microarrays (Human Genome U133 plus 2.0) to compare global gene expression between SARS-CoV-infected, mock-infected and SARS-CoV-ΔE-infected cells. For ech type of sample three hybridizations were carried-out (independent biological replicates).
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Project description:The amount of SARS-CoV-2 detected in the upper respiratory tract (URT viral load) is a key driver of transmission of infection. Current evidence suggests that mechanisms constraining URT viral load are different from those controlling lower respiratory tract viral load and disease severity. Understanding such mechanisms may help to develop treatments and vaccine strategies to reduce transmission. Combining mathematical modelling of URT viral load dynamics with transcriptome analyses we aimed to identify mechanisms controlling URT viral load. COVID-19 patients were recruited in Spain during the first wave of the pandemic. RNA sequencing of peripheral blood and targeted NanoString nCounter transcriptome analysis of nasal epithelium were performed and gene expression analysed in relation to paired URT viral load samples collected within 15 days of symptom onset. Proportions of major immune cells in blood were estimated from transcriptional data using computational differential estimation. Weighted correlation network analysis (adjusted for cell proportions) and fixed transcriptional repertoire analysis were used to identify associations with URT viral load, quantified as standard deviations (z-scores) from an expected trajectory over time.
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Project description:To further investigate the underlying mechanisms of severe acute respiratory syndrome (SARS) pathogenesis and evaluate the therapeutic efficacy of potential drugs and vaccines it is necessary to use an animal model that is highly representative of the human condition in terms of respiratory anatomy, physiology and clinical sequelae. The ferret, Mustela putorius furo, supports SARS-CoV replication and displays many of the symptoms and pathological features seen in SARS-CoV-infected humans. We have recently established a SARS-CoV infection-challenge ferret platform for use in evaluating potential therapeutics to treat SARS. The main objective of the current study was to extend our previous results and identify early host immune responses upon infection and determine immune correlates of protection upon challenge with SARS-CoV in ferrets. Keywords: time course This study is a simple time course (58 day) examination of host responses in 35 SARS-CoV (TOR2) infected ferrets with the addition of a challenge inoculation of SARS CoV (TOR2) at day 29 post infection. Three mock-infected ferrets are included as negative controls. Due to the unavailability of ferret microarrays, Affymetrix Canine 2.0 oligonucleotide arrays were chosen following sequence analysis of our ferret cDNA library (~5000 clones) and demonstration of high levels of homology (>80%) between dog and ferret.
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