SARS-CoV-2 infection of human pancreatic islets
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ABSTRACT:
PROVIDER: PRJNA670242 | ENA |
REPOSITORIES: ENA
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Project description:Several studies have suggested a relationship between SARS-CoV-2 infection and diabetes. This study examined the consequences of infection of human pancreatic islets with SARS-CoV-2 virus. This GEO submission contains the raw and processed data from single-cell RNA sequencing (scRNAseq) experiments evaluating the tropism of SARS-CoV-2 in pancreatic islets and transcriptional changes induced by infection of these cells. Overall we observed limited infection of pancreatic islets (0.2 - 3.4% of all cells infected per donor) and identified multiple pancreatic cell types as targets of infection; due to the preponderance of major endocrine cell populations in our islet cell preparations, downstream analyses were primarily focused on alpha and beta cells. Within beta cells we identified an upregulation of interferon stimulated genes in both infected and bystander cells as well as an NFκB mediated genes in infected cells only. Within alpha cells we detected a non-specific downregulation of a large number of host genes in infected cells.
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Project description:Recent clinical data has suggestedsed a bi-directional relationship between Coronavirus disease 19 (COVID-19) and diabetes. Here, we showdemonstrateed the detection of SARS-CoV-2 in pancreatic endocrine cells in autopsy samples derived fromof COVID-19 patients. Single cell RNA-seq and immunostaining confirmed that multiple types of pancreatic islet cells can be infected byare susceptible to SARS-CoV-2, eliciting a cellular stress response and the induction of chemokines. SARS-CoV-2 infection causes the increase of chemokine response, cell stress, and interferon signal. Upon SARS-CoV-2 infection, beta cells show a the decreased expression of insulin and the increased expression of alpha and acinar cell markers, including glucagon and , and acinar cell markers, including PRSS1/trypsin1, respectfully, suggesting which suggests that infected beta cells undergocellular dedifferentiation. This was furtherCorroboration of these findings could be further validated using theinex vivo using single cell sequencing of pancreatic tissue from autopsy of COVID-19 patients autopsies. Trajectory analysis identifiedindicated that the EIF2 pathway that changess along withmediates beta cell dedifferentiation. Furthermore, a, and a high content screen identified trans-integrated stress response inhibitor (trans-ISRIB) that as decreasinges poly-hormonal cells. Finally, trans-ISRIB treatmentwhich rescueds beta cell dedifferentiation upon SARS-CoV-2 exposure. Together, it, suggestings that SARS-CoV-2 infection causes EIF2 pathway-mediated beta cell dedifferentiation. Altogether, tThis study provides a potential mechanism of new onset diabetes in upon the development of COVID-19.
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Project description:The SARS-CoV-2 virus has already caused over a million COVID-19 cases and over fifty-thousand deaths globally. There is an urgent need to create novel models to study SARS-CoV-2 virus using human disease-relevant cells and tissues to understand key features of virus biology. We present a platform comprised of nine different cell and organoid derivatives from human pluripotent stem cells (hPSCs) representing all three primary germ layers, including lung progenitors and alveolar type II (AT2) cells, pancreatic endocrine cells, liver organoids, endothelial cells, cardiomyocytes, macrophages, microglia, and both cortical and dopaminergic neurons. We systematically probed which cell types are permissive to SARS-CoV-2 infection. Human pancreatic beta cells and hepatocytes were strikingly permissive to SARS-CoV-2 infection, further validated using adult primary human islets and liver organoids. Both in vitro and in a humanized mouse model, human lung progenitors and AT2 cells express the ACE2 viral receptor and were highly permissive to SARS-CoV-2 infection. Transcriptomic analysis following SARS-CoV-2 infection of hPSC-derived pancreatic and lung organoids revealed upregulation of chemokines but not type I/III interferon signaling, similar to what was seen in primary human COVID-19 pulmonary infection. Therefore, hPSC-derived cells phenocopy human COVID-19 disease and provide a valuable resource to understand SARS-CoV-2 biology and search for novel therapeutics.
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Project description:Healthcare workers were recruited at St Bartholomew’s Hospital, London, UK in the week of lockdown in the United Kingdom (between 23rd and 31st March 2020). Participants underwent weekly evaluation using a questionnaire and biological sample collection (including serological assays) for up to 16 weeks when attending for work and self-declared as fit to attend work at each visit, with further follow up samples collected at 24 weeks. Blood RNA sequencing data was to be used to identify host-response biomarkers of early SARS-CoV-2 infection, to evaluate existing blood transcriptomic signatures of viral infection, and to describe the underlying biology during SARS-CoV-2 infection. This submission includes a total of 172 blood RNA samples from 99 participants. Of these, 114 samples (including 16 convalescent samples collected 6 months after infection) were obtained from 41 SARS-CoV-2 cases, with the remaining 58 from uninfected controls. Participants with available blood RNA samples who had PCR-confirmed SARS-CoV-2 infection during follow-up were included as ‘cases’. Those without evidence of SARS-CoV-2 infection on nasopharyngeal swabs and who remained seronegative by both Euroimmun anti S1 spike protein and Roche anti nucleocapsid protein throughout follow-up were included as uninfected controls. ‘Cases’ include all available RNA samples, including convalescent samples at week 24 of follow-up for a subset of participants. For uninfected controls, we included baseline samples only. Sample class denotes weekly interval to positive SARS-CoV-2 PCR; non-infected controls (NIC); convalescent samples (Conv)_.
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