{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Triana S"],"funding":["Deutsche Forschungsgemeinschaft (DFG)","Bundesministerium für Bildung und Forschung","Deutsche Forschungsgemeinschaft","European Research Council","Bundesministerium für Bildung und Forschung (BMBF)","DAAD"],"pagination":["e10232"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8077299"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(4)"],"pubmed_abstract":["Exacerbated pro-inflammatory immune response contributes to COVID-19 pathology. However, despite the mounting evidence about SARS-CoV-2 infecting the human gut, little is known about the antiviral programs triggered in this organ. To address this gap, we performed single-cell transcriptomics of SARS-CoV-2-infected intestinal organoids. We identified a subpopulation of enterocytes as the prime target of SARS-CoV-2 and, interestingly, found the lack of positive correlation between susceptibility to infection and the expression of ACE2. Infected cells activated strong pro-inflammatory programs and produced interferon, while expression of interferon-stimulated genes was limited to bystander cells due to SARS-CoV-2 suppressing the autocrine action of interferon. These findings reveal that SARS-CoV-2 curtails the immune response and highlights the gut as a pro-inflammatory reservoir that should be considered to fully understand SARS-CoV-2 pathogenesis."],"journal":["Molecular systems biology"],"pubmed_title":["Single-cell analyses reveal SARS-CoV-2 interference with intrinsic immune response in the human gut."],"pmcid":["PMC8077299"],"funding_grant_id":["416072091","272983813","01KI20198A","240245660","773089","415089553","278001972","01KI20239B","57440921"],"pubmed_authors":["Boulant S","Metz-Zumaran C","Herrmann C","Sharma AK","Shahraz M","Schraivogel D","Gschwind AR","Alexandrov T","Ramirez C","Steinmetz LM","Stanifer ML","Triana S","Doldan P","Kee C"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell analyses reveal SARS-CoV-2 interference with intrinsic immune response in the human gut.","description":"Exacerbated pro-inflammatory immune response contributes to COVID-19 pathology. However, despite the mounting evidence about SARS-CoV-2 infecting the human gut, little is known about the antiviral programs triggered in this organ. To address this gap, we performed single-cell transcriptomics of SARS-CoV-2-infected intestinal organoids. We identified a subpopulation of enterocytes as the prime target of SARS-CoV-2 and, interestingly, found the lack of positive correlation between susceptibility to infection and the expression of ACE2. Infected cells activated strong pro-inflammatory programs and produced interferon, while expression of interferon-stimulated genes was limited to bystander cells due to SARS-CoV-2 suppressing the autocrine action of interferon. These findings reveal that SARS-CoV-2 curtails the immune response and highlights the gut as a pro-inflammatory reservoir that should be considered to fully understand SARS-CoV-2 pathogenesis.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2026-05-08T21:28:40.424Z","creation":"2022-02-10T14:47:39.862Z"},"accession":"S-EPMC8077299","cross_references":{"pubmed":["33904651"],"doi":["10.15252/msb.202110232"]}}