Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ScRNAseq of human primary nasal epithelium differentiated at air-liquid interface exposed to SARS-CoV2

ABSTRACT: The nasal epithelium is a plausible entry point for SARS-CoV-2, a site of pathogenesis and transmission, and may initiate the host response to SARS-CoV-2. Antiviral interferon responses are critical to outcome of SARS-CoV-2. Yet little is known about the interaction between SARS-CoV-2 and innate immunity in this tissue. Here we applied single-cell RNA sequencing and proteomics to a primary cell model of human primary nasal epithelium differentiated at air-liquid interface.

PROVIDER: EGAS00001005633 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

Phosphoproteome of SARS-CoV-2 infected Human Nasal Epithelium

Project description:The nasal epithelium is the primary initial site of SARS-CoV-2 entry in the human body. Since much of the molecular detail defining coronavirus entry and replication was derived from non-nasal cell lines, it remains unclear how SARS-CoV-2 overcomes the physical nasal mucus and periciliary mucin layers to infect and spread through the nasal epithelium. Using air-liquid interface cultured primary nasal epithelial cells, we observed that SARS-CoV-2 attaches to motile cilia during the initial stage of infection. Depletion of cilia inhibited SARS-CoV-2, as well as respiratory syncytial virus and parainfluenza virus infection, suggesting a widely-used ciliary mechanism for respiratory viral entry. Using electron and immunofluorescence microscopy, we further observed that SARS-CoV-2 progeny virions attached to airway microvilli 24 hours post infection and triggered the formation of apically extended and highly branched microvilli that organize viral egress from the microvillar base back into the mucus layer, supporting a model of virus dispersion throughout airway tissue via mucociliary transport. Chemical perturbation of microvillus formation severely impaired viral egress and subsequent spread. Phosphoproteomic analyses indicate that virally-triggered microvillar branching is linked to the p21-activated kinase 1 and 4 (PAK1/4) signaling pathway and viral infection is impaired by PAK1/4 kinase inhibitors. Our work provides insight into the mechanisms by which SARS-CoV-2 and potentially many respiratory viruses penetrate the physical nasal epithelium barrier, a first line of defense against pathogens, thus revealing a new view of the motile cilia and microvilli as critical host factors required for viral entry and egress.

2023-03-10 | PXD028123 | Pride

Leander2021 - innate immune response to SARS-CoV-2 in the alveolar epithelium

Project description:A mathematical ODE based model of the innate immune response to SARS-CoV-2 in the alveolar epithelium.

2021-11-17 | MODEL2111170001 | BioModels

Interferon signaling in the nasal epithelium distinguishes among lethal and common cold respiratory viruses and is critical for viral clearance

Project description:All respiratory viruses establish primary infections in the nasal epithelium, where efficient innate immune induction may prevent dissemination to the lower airway and thus minimize pathogenesis. Human coronaviruses (HCoVs) cause a range of pathologies, but the host and viral determinants of disease during common cold versus lethal HCoV infections are poorly understood. We model the initial site of infection using primary nasal epithelial cells cultured at air-liquid interface (ALI). HCoV-229E, HCoV-NL63 and human rhinovirus-16 are common cold-associated viruses that exhibit unique features in this model: early induction of antiviral interferon (IFN) signaling, IFN-mediated viral clearance, and preferential replication at nasal airway temperature (33ºC) which confers muted host IFN responses. In contrast, lethal SARS-CoV-2 and MERS-CoV encode antagonist proteins that prevent IFN-mediated clearance in nasal cultures. Our study identifies features shared among common cold-associated viruses, highlighting nasal innate immune responses as predictive of infection outcomes and nasally-directed IFNs as potential therapeutics.

2024-03-25 | GSE253542 | GEO

RNA-Seq of SARS-Cov-2 Infection in Human Airway Epithelium Organoids

Project description:We performed RNA-Seq of SARS-Cov-2 infection in human airway epithelium organoids. The organoids were infected with SARS-Cov-2 for 24hours or 48hours respectively, and compared with uninfected mock control.

2021-08-07 | GSE155974 | GEO

RNA-Seq of SARS-Cov-2 Infection in Human Bronchial Epithelium Organoids

Project description:We performed RNA-Seq of SARS-Cov-2 infection in human bronchial epithelium organoids. The organoids were infected with SARS-Cov-2 for 48hours or 72hours respectively, and compared with uninfected mock control.

2021-06-08 | GSE152060 | GEO

Capturing SARS-cov in low abundant patient samples: a comparative analysis (twist panviral NS).

Project description:In this study, we tested the efficacy of five commercial probes panels at detecting SARS-CoV-2 genome including panels from Illumina, Twist Bioscience and Arbor Bioscience. To do so, we used 19 patient nasal swab samples broken down into 5 series of 4 samples of equivalent SARS-CoV-2 viral load (cycle threshold (CT): low CT means a high viral load – CT26, CT29, CT32, CT35 and CT36+).

2022-06-01 | E-MTAB-11237 | biostudies-arrayexpress

Capturing SARS-cov in low abundant patient samples: a comparative analysis (arbo double ms) .

2022-06-01 | E-MTAB-11232 | biostudies-arrayexpress

Capturing SARS-cov in low abundant patient samples: a comparative analysis (Illumina respv NS).

2022-02-08 | E-MTAB-11233 | biostudies-arrayexpress

Capturing SARS-cov in low abundant patient samples: a comparative analysis (Twist sarscov MS).

2022-06-01 | E-MTAB-11234 | biostudies-arrayexpress

Capturing SARS-cov in low abundant patient samples: a comparative analysis (arbo single MS).

2022-06-01 | E-MTAB-11235 | biostudies-arrayexpress