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Modeling SARS-CoV-2 infection and its individual differences with ACE2-expressing human iPS cells

ABSTRACT: Modeling SARS-CoV-2 infection and its individual differences with ACE2-expressing human iPS cells

PROVIDER: PRJNA702533 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13734378.fastq.gz	Fastqsanger.gz
	SRR13734379.fastq.gz	Fastqsanger.gz
	SRR13734380.fastq.gz	Fastqsanger.gz
	SRR13734381.fastq.gz	Fastqsanger.gz
	SRR13734382.fastq.gz	Fastqsanger.gz

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Modeling SARS-CoV-2 infection and its individual differences with ACE2-expressing human iPS cells

Project description:Genetic differences are a primary reason for differences in the susceptibility and severity of COVID-19. As induced pluripotent stem (iPS) cells maintain the genetic information of the donor, they can be used to model individual differences in SARS-CoV-2 infection in vitro. We found that human iPS cells expressing the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) (ACE2-iPS cells) can be infected w SARS-CoV-2. In infected ACE2-iPS cells, the expression of SARS-CoV-2 nucleocapsid protein, budding of viral particles, and production of progeny virus, double membrane spherules, and double-membrane vesicles were confirmed. We performed SARS-CoV-2 infection experiments on ACE2-iPS/ embryonic stem (ES) cells from eight individuals. Male iPS/ES cells were more capable of producing the virus compared with female iPS/ES cells. These findings suggest that ACE2-iPS cells can not only reproduce individual differences in SARS-CoV-2 infection in vitro but also are a useful resource to clarify the causes of individual differences in COVID-19 due to genetic differences.

2021-04-18 | GSE166990 | GEO

Modeling SARS-CoV-2 infection and its individual differences with ACE2-expressing human iPS cells.

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ACE2 knockout hinders SARS-CoV-2 propagation in iPS cell-derived airway and alveolar epithelial cells

Project description:Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the causative agent of COVID-19, continues to spread around the world with serious cases and deaths. It has also been suggested that different genetic variants in the human genome affect both the susceptibility to infection and severity of disease in COVID-19 patients. Angiotensin-converting enzyme 2 (ACE2) has been identified as a cell surface receptor for SARS-CoV and SARS-CoV-2 entry into cells. The construction of an experimental model system using human iPS cells would enable further studies of the association between viral characteristics and genetic variants. Airway and alveolar epithelial cells are cell types of the lung that express high levels of ACE2 and are suitable for in vitro infection experiments. Here, we show that human iPS cell-derived airway and alveolar epithelial cells are highly susceptible to viral infection of SARS-CoV-2. Using gene knockout with CRISPR-Cas9 in human iPS cells we demonstrate that ACE2 plays an essential role in the airway and alveolar epithelial cell entry of SARS-CoV-2 in vitro. Replication of SARS-CoV-2 was strongly suppressed in ACE2 knockout (KO) lung cells. Our model system based on human iPS cell-derived lung cells may be applied to understand the molecular biology regulating viral respiratory infection leading to potential therapeutic developments for COVID-19 and the prevention of future pandemics.

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Project description:The aim was to study the effect of 1) coculture of iPS-ECs and iPS-CMs on each cell type and 2) shear stress on iPS-derived endothelial cells (iPS-EC). The transcriptional landscapes of each cell type were compared.

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