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Human organoid systems reveal in vitro correlates of fitness for SARS-CoV-2 B.1.1.7

ABSTRACT: Human organoid systems reveal in vitro correlates of fitness for SARS-CoV-2 B.1.1.7

PROVIDER: PRJNA738504 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14850601.fastq.gz	Fastqsanger.gz
	SRR14850602.fastq.gz	Fastqsanger.gz
	SRR14850603.fastq.gz	Fastqsanger.gz
	SRR14850604.fastq.gz	Fastqsanger.gz
	SRR14850605.fastq.gz	Fastqsanger.gz

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Human organoid systems reveal in vitro correlates of fitness for SARS-CoV-2 B.1.1.7

Project description:A new phase of the COVID-19 pandemic has started as SARS-CoV-2 variants with increased transmissibility are emerging globally, calling for the development of reliable platforms to rapidly phenotype viruses. Currently, no rapid phenotyping system exists that both accurately models human biology and can be standardized properly. Organoids accurately model viral target cells in vivo, can be established from many tissues, passaged indefinitely, biobanked and shared. We found that the British variant (clade B.1.1.7), compared to an ancestral 614G-containing clade B virus, produced higher levels of infectious virus late in infection and had a higher replicative fitness in human airway, alveolar and intestinal organoid models. Our findings unveil extended shedding as a correlate of fitness for SARS-CoV-2, possibly explaining the rapid emergence of SARS-CoV-2 B.1.1.7. Combined with genomic surveillance systems, virus phenotyping using standardized organoid models may be implemented into public health decision making.

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Aneuploidy tolerance caused by BRG1 loss allows gain of chromosome 18 and improved fitness

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High-Resolution CRISPR Screens Reveal Fitness Genes and Genotype-Specific Cancer Liabilities

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Project description:T-cell dysfunction genes limit antitumor activity and may serve as therapeutic targets. It has not been systematically studied whether there are regulators that either uniquely or broadly contribute to T-cell fitness. We performed genome-scale CRISPR/Cas9 knockout screens in primary CD8 T-cells to uncover genes negatively impacting on fitness upon three modes of stimulation: (1) intense stimulation, triggering activation-induced cell death (AICD); (2) acute stimulation, triggering T-cell expansion; (3) chronic stimulation, causing dysfunction. Besides established regulators, we uncovered genes controlling T-cell fitness either specifically or commonly upon differential stimulation. Dap5 ablation, ranking highly in all three screens, increased translation while enhancing tumor killing. Loss of Icam1-mediated homotypic T-cell clustering amplified T-cell expansion and effector functions after both acute and intense stimulation. Lastly, Ctbp1 inactivation induced functional T-cell persistence exclusively upon chronic stimulation. Our results functionally annotate fitness regulators based on their unique or shared contribution to traits limiting T-cell antitumor activity.

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Multimodal stimulation screens reveal unique and shared regulators limiting T-cell fitness [Ctbp1]

Project description:It has not been systematically studied whether T-cell fitness regulators uniquely or broadly contribute to specific traits limiting antitumor activity. We performed genome-scale CRISPR/Cas9 knockout screens in primary CD8 T-cells to uncover genes negatively impacting on their fitness upon three modes of stimulation: (1) intense stimulation, causing activation-induced cell death (AICD); (2) acute stimulation, triggering T-cell expansion; (3) chronic stimulation, resulting in dysfunction. Besides established regulators, we uncovered several genes controlling T-cell fitness either specifically or commonly under various stimulation modalities. Ablation of Dap5, ranking highly in all three screens, increased translation while enhancing tumor killing. Loss of Icam1-mediated homotypic T-cell clustering amplified T-cell expansion and effector functions after both acute and intense stimulation. Finally, inactivation of Ctbp1 induced T-cell persistence exclusively upon chronic stimulation. Our results functionally annotate T-cell fitness regulators based on their unique or shared contribution to traits limiting T-cell antitumor activity.

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