Characterization of the SARS-CoV-2 Host Response in Primary Human Airway Epithelial Cells from Aged Individuals
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ABSTRACT:
PROVIDER: PRJNA733520 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14682600.fastq.gz | Fastqsanger.gz | |||
| SRR14682601.fastq.gz | Fastqsanger.gz | |||
| SRR14682602.fastq.gz | Fastqsanger.gz | |||
| SRR14682603.fastq.gz | Fastqsanger.gz | |||
| SRR14682604.fastq.gz | Fastqsanger.gz |
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Project description:Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the causative agent of coronavirus disease 2019 (COVID-19), a global pandemic characterized by respiratory illness and an exaggerated immune response. Age (>60 years) is a significant risk factor for developing severe COVID-19. However, the underlying mechanisms of how aging impacts SARS-CoV-2 infection and the host response are largely unknown. Therefore, we performed an in vitro study to characterize the host response to SARS-CoV-2 infection using primary human bronchial epithelial cells from donors >67 years of age differentiated on air-liquid interface culture. We demonstrate that SARS-CoV-2 infection leads to early induction of a proinflammatory response and a delayed interferon response. In addition, we observe changes in genes and pathways associated with cell death and senescence throughout infection. In summary, our study provides important insights into the temporal kinetics of the airway epithelial innate immune response to SARS-CoV-2 in older individuals.
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Project description:Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the causative agent of coronavirus disease 2019 (COVID-19), a global pandemic characterized by an exaggerated immune response and respiratory illness. Age (>60 years) is a significant risk factor for developing severe COVID-19. To better understand the host response of the aged airway epithelium to SARS-CoV-2 infection, we performed an in vitro study using primary human bronchial epithelial cells from donors >67 years of age differentiated on an air-liquid interface culture. We demonstrate that SARS-CoV-2 infection leads to early induction of a proinflammatory response and a delayed interferon response. In addition, we observed changes in the genes and pathways associated with cell death and senescence throughout infection. In summary, our study provides new and important insights into the temporal kinetics of the airway epithelial innate immune response to SARS-CoV-2 in older individuals.
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Project description:For the assessment of host response dynamics to SARS-CoV and SARS-CoV-2 infections in human airway epithelial cells at ambient temperature corresponding to the upper or lower respiratory tract. We performed a temporal transcriptome analysis on human airway epithelial cell (hAEC) cultures infected with SARS-CoV and SARS-CoV-2, as well as uninfected hAEC cultures, incubated either at 33°C or 37°C. hAEC cultures were harvested at 24, 48 72, 96 hpi and processed for Bulk RNA Barcoding and sequencing (BRB-seq), which allows a rapid and sensitive genome-wide transcriptomic analysis in a highly multiplexed manner. Transcriptome data was obtained from a total of 7 biological donors for pairwise comparisons of SARS-CoV or SARS-CoV-2 virus-infected to unexposed hAEC cultures at respective time points and temperatures.
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