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Single cell susceptibility to SARS-CoV-2 infection is driven by variable cell states [scRNA-Seq]

ABSTRACT: Single cell susceptibility to SARS-CoV-2 infection is driven by variable cell states [scRNA-Seq]

PROVIDER: PRJNA993165 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25224300.fastq.gz	Fastqsanger.gz
	SRR25224297.fastq.gz	Fastqsanger.gz
	SRR25224298.fastq.gz	Fastqsanger.gz
	SRR25224299.fastq.gz	Fastqsanger.gz

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Single cell susceptibility to SARS-CoV-2 infection is driven by variable cell states

Project description:Single cell susceptibility to SARS-CoV-2 infection is driven by variable cell states

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Single cell susceptibility to SARS-CoV-2 infection is driven by variable cell states [bulkRNA-Seq]

Project description:Single cell susceptibility to SARS-CoV-2 infection is driven by variable cell states [bulkRNA-Seq]

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Single cell susceptibility to SARS-CoV-2 infection is driven by variable cell states [bulkRNA-Seq]

Project description:The ability of a virus to infect a cell type is partly determined by host factors required for the viral life cycle. However, not every cell of a given type is equally susceptible, suggesting that our knowledge of the full spectrum of factors that promote infection is incomplete. Profiling the susceptible subsets of cells could reveal additional host factors, but viral infection dramatically alters the state of the cell, obscuring the state of these cells prior to infection. We used single-cell clone tracing to retrospectively identify cells that were highly susceptible to infection with SARS-CoV-2. Our approach revealed candidate factors playing roles in viral entry and regulation of the infectable cell state itself. Patient samples revealed heterogeneous expression of these factors in vivo, with heightened expression in particular inflammatory pathologies. Thus, variable expression of intrinsic cell states is a major determinant of whether individual cells can be infected by SARS-CoV-2.

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Single cell susceptibility to SARS-CoV-2 infection is driven by variable cell states [scRNA-Seq]

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Single cell susceptibility to SARS-CoV-2 infection is driven by variable cell states

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Single-cell sequencing of glioblastoma reveals central nervous system susceptibility to SARS-CoV-2

Project description:Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the recent global COVID-19 outbreak, which led to a public health emergency. Entry of SARS-CoV-2 into human cells is dependent on the SARS-CoV receptor, angiotensin converting enzyme 2 (ACE2) receptor, and cathepsin. Cathepsin degrades the spike protein (S protein), which results in the entry of viral nucleic acid into the human host cell. Methods: We explored the susceptibility of the central nervous system (CNS) to SARS-CoV-2 infection using single-cell transcriptome analysis of glioblastoma. Results: The results showed that ACE2 expression is relatively high in endothelial cells (ECs), bone marrow mesenchymal stem cells (BMSCs), and neural precursor cells (NPCs). Cathepsin B (Cat B) and cathepsin (Cat L) were also strongly expressed in various cell clusters within the glioblastoma microenvironment. Immunofluorescence staining of glioma and normal brain tissue chips further confirmed that ACE2 expression co-localized with CD31, CD73, and nestin, which confirmed the susceptibility to SARS-CoV-2 of nervous system cells, including ECs, BMSCs and NPCs, from clinical specimens. Conclusions: These findings reveal the mechanism of SARS-CoV-2 neural invasion and suggest that special attention should be paid to SARS-CoV-2-infected patients with neural symptoms, especially those who suffered a glioma.

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A chemically-targetable transcription factor-chromatin remodeler interaction underlies SARS-CoV-2 susceptibility

Project description:Identification of host determinants of coronavirus infection informs mechanisms of viral pathogenesis and provides novel therapeutic targets. Here, we demonstrate that the mSWI/SNF chromatin remodeling complex promotes coronavirus infection and represents a host-directed therapeutic target. SMARCA4 catalytic activity is required for mSWI/SNF-driven chromatin accessibility at the ACE2 locus, which is essential for ACE2 expression and virus susceptibility. Recruitment of mSWI/SNF complexes to ACE2 is mediated by mSWI/SNF binding to the transcription factor, HNF1A, enabling complex occupancy and chromatin accessibility at sites containing high HNF1A motif density. Notably, small molecule inhibition of mSWI/SNF catalytic activity abrogates ACE2 expression confers resistance to SARS-CoV-2 variants and infection of primary human airway cells by 5-logs. These data highlight the role for mSWI/SNF-mediated chromatin remodeling activities in conferring SARS-CoV-2 susceptibility and identify a potential new class of inhibitors to combat COVID-19.

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Project description:Gastrointestinal effects associated with Coronavirus Disease 2019 (COVID-19) are highly variable for reasons that are not understood. In this study, we used intestinal organoid-derived cultures differentiated from primary human specimens as a model to examine interindividual variability. Infection of intestinal organoids derived from different donors with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) resulted in orders of magnitude differences in virus replication in small intestinal and colonic organoid-derived monolayers. Susceptibility to infection correlated with angiotensin I converting enzyme 2 (ACE2) expression level and was independent of donor demographic or clinical features. ACE2 transcript levels in cell culture matched the amount of ACE2 in primary tissue, indicating that this feature of the intestinal epithelium is retained in the organoids. Longitudinal transcriptomics of organoid-derived monolayers identified a delayed yet robust interferon signature, the magnitude of which corresponded to the degree of SARS-CoV-2 infection. Interestingly, virus with the Omicron variant spike (S) protein infected the organoids with the highest infectivity, suggesting increased tropism of the virus for intestinal tissue. These results suggest that heterogeneity in SARS-CoV-2 replication in intestinal tissues results from differences in ACE2 levels, which may underlie variable patient outcomes.

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