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Human embryonic stem cell-derived cardiomyocytes express SARS-CoV-2 host entry proteins

ABSTRACT: Human embryonic stem cell-derived cardiomyocytes express SARS-CoV-2 host entry proteins: screen to identify inhibitors of infection

PROVIDER: PRJEB48328 | ENA |

REPOSITORIES: ENA

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Human embryonic stem cell-derived cardiomyocytes express SARS-CoV-2 host entry proteins

Project description:Human embryonic stem cell-derived cardiomyocytes express SARS-CoV-2 host entry proteins: screen to identify inhibitors of infection

| PRJEB43469 | ENA

Differential Whole Genome CRISPR Screening Strategy for SARS-CoV-2 Spike and VSV-G Mediated Pseudoviral Entry

Project description:The coronavirus disease 2019 (COVID-19) has caused over 6 million deaths worldwide and disrupted the global economy. The causative agent for this disease, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes mild to lethal respiratory infections. Understanding the cellular host factors that promote and inhibit for SARS-CoV-2 infection is important for identifying virial countermeasures. Moreover, new methods are needed to be to identify host genes influencing specific steps of viral infections. Here, we developed a CRISPR whole genome screen against SARS-CoV-2 spike enveloped retro-pseudoviruses with a GFP reporter to specifically identify host genes that facilitate viral entry. By including two counter screen strategies, this approach can be used to distinguish host genes affecting the pseudoviral reporter from those unique to envelope-mediated entry. First, an alternate envelope, VSV-G allowed identification of shared genes associated with retro-transcription, integration and reporter expression. Second, a recently developed Cre-Gag fusion pseudovirus bypassed retro transcription and integration by directly activating a floxed GFP reporter. Our approach correctly identified SARS-CoV-2 and VSV-G receptors ACE2 and LDLR, respectively and distinguished genes associated with retroviral reporter expression from envelope mediated entry. Overall, this work provides a new strategy for screening genes influencing envelope mediated entry without the complexity of live-viral screens which are complicated with large numbers of genes associated with all aspects of viral pathogenesis and replication. This approach should be of use for identifying genes contributing to and inhibiting SARS-CoV-2 entry and provide a platform for the analysis of newly emerging viruses.

2022-06-27 | GSE206996 | GEO

ACE2-independent SARS-CoV-2 virus entry through cell surface GRP78 on monocytes - evidence from a translational clinical and experimental approach

Project description:SARS-CoV-2 infects host cells via an ACE2/TMPRSS2 entry mechanism. Monocytes and macrophages, which play a key role during severe COVID-19 express only low or no ACE2, suggesting alternative entry mechanisms in these cells. In silico analyses predicted GRP78, which is constitutively expressed on monocytes and macrophages, to be a potential candidate receptor for SARS-CoV-2 virus entry. To confirm the hypothesis, we conducted high-throughput RNA sequence to characterize the role of GRP78 in monocytes function in COVID-19 patients

2023-12-13 | GSE245922 | GEO

Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia (scRNA-seq: olfactory mucosa)

Project description:A subset of COVID-19 patients exhibit altered olfactory function. Here we analyze bulk and single cell RNA-Seq datasets to identify cell types in the olfactory epithelium and olfactory bulb that express cell entry molecules that mediate infection by SARS-CoV-2 (CoV-2), the causal agent in COVID-19. We find that samples from whole olfactory mucosa in species including mouse and human express two key genes involved in CoV-2 entry, ACE2 and TMPRSS2. However, neither olfactory sensory neurons nor olfactory bulb neurons express these genes, which are instead expressed in support cells, stem cells, and perivascular cells. These findings suggest that CoV-2 infection of non-neuronal cell types leads to anosmia and related disturbances in odor perception in COVID-19 patients.

2020-07-30 | GSE151346 | GEO

Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia (scRNA-seq: olfactory bulb)

2020-07-30 | GSE148360 | GEO

Genome-wide transcriptomic profiling of human iPS-derived cardiomyocytes in response to ectopic expression of SARS-CoV-2 proteins

Project description:In this study, we investigated the effects of SARS-CoV-2 subunits on cardiomyocytes derived from human stem cells. The human induced pluripotent stem cells (hiPSCs) was differentiated into cardiomyocytes, and then were transfected with plasmids carrying different SARS-CoV-2 subunits. The cardiac functions, such as contractility and metabolic profiles, were investigated. We found the subunits 9B and S proteins has significantly adversed effects on the cardiac functions, compared to other groups. Thus, changes in transcriptome of cardiomyocytes (day30) after over expression of 9B, S for two days (on day 32) and two weeks (on day 45) were investigated by RNA-seq.

2023-02-02 | GSE202869 | GEO

Orai-mediated calcium entry regulates the excitability of central dopaminergic neurons

Project description:Transcriptomic screen from Drosophila pupal CNS to identify genes regulated by loss of Orai-mediated Ca2+ entry in a subset of dopaminergic neurons by means of expression of the OraiE180A dominan negative allele

2024-01-25 | GSE230134 | GEO

Repression of OSMR and FGFR1 by miR-1/133a prevents adult cardiomyocyte dedifferentiation and cell cycle entry in the adult heart

Project description:Deletion of the miR-1/133a clusters in adult cardiomyocytes results in upregulation of miRNA target genes FGFR1 and OSMR. Additional deletion of these miRNA target genes reveals a co-operative role of these receptors in the control of the cardiomyocyte differentiation state and in repression of cardiomyocyte cell cycle re-entry.

2021-09-17 | E-MTAB-10226 | biostudies-arrayexpress

Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages [scRNA-seq dataset]

Project description:Heart injury has been reported in up to 20% of COVID-19 patients, yet the cause of myocardial histopathology is unknown. We examined heart tissue from autopsies of healthy and COVID-19 patients using RNA-seq and identified a strikingly increased CCL2 expression and macrophage population in COVID-19 heart sample. Transwell assays using hESC-derived cardiomyocytes (CMs) and macrophages revealed that SARS-CoV-2 infected CMs secrete CCL2, which recruits macrophages, and this was validated using adult human CMs. Macrophages recruited by CCL2 from infected CMs secrete IL-6 and TNF-α, which causes increased ROS and cell apoptosis of CMs. Finally, a high content chemical screen using FDA-approved drugs identified ranolozine and tofacitinib, which rescue SARS-CoV-2 infected CMs from macrophages-induced cardiotoxicity.

2020-10-29 | GSE151878 | GEO

Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages [bulk RNA-seq dataset)

2020-10-29 | GSE151879 | GEO