{"database":"EGA","file_versions":[],"scores":null,"additional":{"omics_type":["Genomics"],"study_type":["Epigenetics"],"submitter_keywords":["COVID-19","2019 novel coronavirus infection","SARS-CoV-2","2019-nCoV infection","severe acute respiratory syndrome coronavirus 2","coronavirus disease 2019","SARS-coronavirus 2"],"full_dataset_link":["https://ega-archive.org/studies/EGAS00001006559"],"host":["EGA"],"description":["EGA study EGAS00001006559"],"dataset_title":["Single-cell omics data for COVID-19 patients"],"repository":["EGA"],"category":["restricted"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell ATAC-seq analysis for COVID19 patients","description":"While SARS-CoV-2 infection causes mild respiratory disease in most individuals, a small group of patients develops severe COVID-19. Dysfunctional innate immune responses have been identified to contribute to differences in COVID-19 severity, but the key regulators are still unknown. Here, we present an integrative single-cell epigenetics, transcriptomic, and genetics analysis of peripheral blood mononuclear cells from hospitalized and convalescent COVID-19 patients. In classical monocytes, we identified 41.3% of significantly up-regulated genes in hospitalized COVID-19 patients potentially induced by differential chromatin accessibility. Sub-clustering and motif-enrichment analyses of monocytes reveal disease condition-specific regulation by transcription factors, such as C/EBPs and SPI1, and their targets, including a long-noncoding RNA LUCAT1, which further regulates interferon responses and is associated with the need for oxygen supply of COVID-19 patients. The interaction between C/EBPs and LUCAT1 was validated through loss-of-function experiments. Finally, we investigated genetic risk variants that exhibit allele-specific open chromatin (ASoC) in promoters/enhancers of COVID-19 patients. Integrating our data with publicly available expression quantitative trait loci and chromosomal interactions indicates that ASoC SNP rs6800484-C is associated with lower expression of CCR2, which may contributeto higher viral loads in lungs and higher risk of COVID-19 hospitalization. Altogether, our study highlights the diverse genetic and epigenetic regulators that contribute to the innate immune responses of different COVID-19 patients.","dates":{"updated":"2022-10-14 14:26:43"},"accession":"EGAS00001006559","cross_references":{"TAXONOMY":["9606"],"OLS":["MONDO_0100096"],"EGA":["EGAD00001009331","EGAC00001002844"]}}