Corpus overview


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MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (105)

ProteinN (6)

ProteinE (3)

NSP5 (2)

ComplexRdRp (1)


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SARS-CoV-2 Proteins
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    scRNA-seq reveals ACE2 HGNC and TMPRSS2 HGNC expression in TROP2 HGNC+ Liver Progenitor Cells: Implications in COVID-19 MESHD associated Liver Dysfunction

    Authors: Justine Jia Wen Seow; Rhea Pai; Archita Mishra; Edwin Shepherdson; Tony Kiat Hon Lim; Brian K P Goh; Jerry KY Chan; Pierce KH Chow; Florent Ginhoux; Ramanuj DasGupta; Ankur Sharma

    doi:10.1101/2020.03.23.002832 Date: 2020-03-25 Source: bioRxiv

    The recent pandemic of coronavirus disease 2019 MESHD ( COVID-19 MESHD) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 MESHD was first reported in China (December 2019) and now prevalent in [~]170 countries across the globe. Entry of SARS-CoV-2 into mammalian cells require the binding of viral Spike (S) proteins PROTEIN to the ACE2 HGNC (angiotensin converting enzyme 2) receptor. Once entered the S protein PROTEIN is primed by a specialised serine protease HGNC, TMPRSS2 HGNC (Transmembrane Serine Protease 2) in the host cell. Importantly, beside respiratory symptoms, consistent with other common respiratory virus infection MESHD when patients become viraemic, a significant number of COVID-19 MESHD patients also develop liver comorbidities. We explored if specific target cell-type in the mammalian liver, could be implicated in disease pathophysiology other than the general deleterious response to cytokine storms. Here we employed single-cell RNA-seq (scRNA-seq) to survey the human liver and identified potentially implicated liver cell-type for viral ingress. We report the co-expression of ACE2 HGNC and TMPRSS2 HGNC in a TROP2 HGNC+ liver progenitor population. Importantly, we fail to detect the expression of ACE2 HGNC in hepatocyte or any other liver (immune and stromal) cell types. These results indicated that in COVID-19 MESHD associated liver dysfunction MESHD and cell death, viral infection of TROP2 HGNC+ progenitors in liver may significantly impaired liver regeneration and could lead to pathology. Highlights- EPCAM HGNC+ Liver progenitors co-express ACE2 HGNC and TMPRSS2 HGNC - ACE2 HGNC and TMPRSS2 HGNC expression is highest in TROP2 HGNChigh progenitors - ACE2 HGNC and TMPRSS2 HGNC cells express cholangiocyte biased fate markers - ACE2 HGNC and TMPRSS2 HGNC positive cells are absent in human fetal liver

    Homology Modeling of TMPRSS2 HGNC Yields Candidate Drugs That May Inhibit Entry of SARS-CoV-2 into Human Cells

    Authors: Stefano Rensi; Russ B Altman; Tianyun Liu; Yu-Chen Lo; Greg McInnes; Alex Derry; Allison Keys

    doi:10.26434/chemrxiv.12009582.v1 Date: 2020-03-20 Source: ChemRxiv

    The most rapid path to discovering treatment options for the novel coronavirus SARS-CoV-2 is to find existing medications that are active against the virus. We have focused on identifying repurposing candidates for the transmembrane serine protease family member II ( TMPRSS2 HGNC), which is critical for entry of coronaviruses into cells. Using known 3D structures of close homologs, we created seven homology models. We also identified a set of serine protease inhibitor drugs, generated several conformations of each, and docked them into our models. We used three known chemical (non-drug) inhibitors and one validated inhibitor of TMPRSS2 HGNC in MERS as benchmark compounds and found six compounds with predicted high binding affinity in the range of the known inhibitors. We also showed that a previously published weak inhibitor, Camostat, had a significantly lower binding score than our six compounds. All six compounds are anticoagulants with significant and potentially dangerous clinical effects and side effects. Nonetheless, if these compounds significantly inhibit SARS-CoV-2 infection MESHD, they could represent a potentially useful clinical tool.

    Analysis the susceptibility of lung cancer patients to SARS-CoV-2 infection MESHD

    Authors: Qi Kong

    doi:10.21203/rs.3.rs-17713/v1 Date: 2020-03-17 Source: ResearchSquare

    Recent studies have reported that 2019 novel coronavirus disease MESHD ( COVID-19 MESHD) patients with lung cancer MESHD have a higher risk of severe events than patients without cancer MESHD. In this study, we investigated the expression of severe acute respiratory syndrome coronavirus 2 (SAR-CoV-2) receptor angiotensin I-converting enzyme 2 ( ACE2 HGNC) and the cellular protease transmembrane serine protease 2 ( TMPRSS2 HGNC) and their associations with prognosis in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma MESHD ( LUSC MESHD). We found that there are significant differences in susceptibility to SAR-CoV-2 among each age stages of individuals with the expression of ACE2 HGNC. ACE2 HGNC was also high expressed in LUAD and LUSC MESHD, and this suggests that COVID-19 MESHD patients with lung cancers MESHD are susceptible to SAR-CoV-2 infection MESHD. Our data showed the differential gene expression level and gene coexpression of ACE2 HGNC and TMPRSS2 HGNC among each subtypes and pathological stages of LUAD and LUSC MESHD and the data were verified by meta-analysis, gene expression omnibus (GEO) data and animal models results. 

    SARS-CoV-2 receptor ACE2 HGNC and TMPRSS2 HGNC are predominantly expressed in a transient secretory cell type in subsegmental bronchial branches

    Authors: Soeren Lukassen; Robert Lorenz Chua; Timo Trefzer; Nicolas C Kahn; Marc A Schneider; Thomas Muley; Hauke Winter; Michael Meister; Carmen Veith; Agnes W Boots; Bianca P Hennig; Michael Kreuter; Christian Conrad; Roland Eils

    doi:10.1101/2020.03.13.991455 Date: 2020-03-14 Source: bioRxiv

    The SARS-CoV-2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID-19 MESHD pathogenesis, especially host factors facilitating virus infection MESHD and replication. SARS-CoV-2 was reported to enter cells via binding to ACE2 HGNC, followed by its priming by TMPRSS2 HGNC. Here, we investigate ACE2 HGNC and TMPRSS2 HGNC expression levels and their distribution across cell types in lung tissue (twelve donors, 39,778 cells) and in cells derived from subsegmental bronchial branches (four donors, 17,521 cells) by single nuclei and single cell RNA sequencing, respectively. While TMPRSS2 HGNC is expressed in both tissues, in the subsegmental bronchial branches ACE2 HGNC is predominantly expressed in a transient secretory cell type. Interestingly, these transiently differentiating cells show an enrichment for pathways related to RHO GTPase function and viral processes suggesting increased vulnerability for SARS-CoV-2 infection MESHD. Our data provide a rich resource for future investigations of COVID-19 MESHD infection and pathogenesis.

    SARS-CoV-2 Entry Genes Are Most Highly Expressed in Nasal Goblet and Ciliated Cells within Human Airways

    Authors: Waradon Sungnak; Ni Huang; Christophe Bécavin; Marijn Berg; HCA Lung Biological Network

    id:2003.06122v1 Date: 2020-03-13 Source: arXiv

    The SARS-CoV-2 coronavirus, the etiologic agent responsible for COVID-19 MESHD coronavirus disease MESHD, is a global threat. To better understand viral tropism, we assessed the RNA expression of the coronavirus receptor, ACE2 HGNC, as well as the viral S protein PROTEIN priming protease TMPRSS2 HGNC thought to govern viral entry in single-cell RNA-sequencing (scRNA-seq) datasets from healthy individuals generated by the Human Cell Atlas consortium. We found that ACE2 HGNC, as well as the protease TMPRSS2 HGNC, are differentially expressed in respiratory and gut epithelial cells. In-depth analysis of epithelial cells in the respiratory tree reveals that nasal epithelial cells, specifically goblet/secretory cells and ciliated cells, display the highest ACE2 HGNC expression of all the epithelial cells analyzed. The skewed expression of viral receptors/entry-associated proteins towards the upper airway may be correlated with enhanced transmissivity. Finally, we showed that many of the top genes associated with ACE2 HGNC airway epithelial expression are innate immune-associated, antiviral genes, highly enriched in the nasal epithelial cells. This association with immune pathways might have clinical implications for the course of infection and viral pathology, and highlights the specific significance of nasal epithelia in viral infection MESHD. Our findings underscore the importance of the availability of the Human Cell Atlas as a reference dataset. In this instance, analysis of the compendium of data points to a particularly relevant role for nasal goblet and ciliated cells as early viral targets and potential reservoirs of SARS-CoV-2 infection MESHD. This, in turn, serves as a biological framework for dissecting viral transmission and developing clinical strategies for prevention and therapy.

    Single-cell RNA expression profiling shows that ACE2 HGNC, the putative receptor of COVID-2019, has significant expression in nasal and mouth tissue, and is co-expressed with TMPRSS2 HGNC and not co-expressed with SLC6A19 HGNC in the tissues

    Authors: Chao Wu; Min Zheng

    doi:10.21203/rs.3.rs-16992/v1 Date: 2020-03-09 Source: ResearchSquare

    A novel coronavirus (COVID-2019) was first identified in Wuhan, Hubei Province, and then spreads to the other Provinces of China. COVID-2019 was reported to share the same receptor, Angiotensin-converting enzyme 2 HGNC ( ACE2 HGNC), with SARS-CoV MESHD. But the infection rate of COVID-2019 is much higher than SARS-CoV MESHD. The biophysical and structural evidence showed that the COVID-2019 binds ACE2 HGNC with 10~20 times affinity than SARS-CoV MESHD. TMPRSS2 HGNC cleaves ACE2 HGNC and facilitates the entry of the virus into host cells. The presence of SLC6A19 HGNC may block the access of TMPRSS2 HGNC to the cutting site on ACE2 HGNC and weaken the entry of COVID-2019 into host cells. Here based on the public single-cell RNA-Seq datasets, we analyzed the ACE2 HGNC expression in the nasal, mouth, lung, and colon tissues. We find that the number of ACE2 HGNC-expressing cells in the nasal and mouth tissues is comparable to the number of ACE2 HGNC-expressing cells in the lung and colon tissues. We also find that ACE2 HGNC tends to be co-expressed with TMPRSS2 HGNC and not co-expressed with SLC6A19 HGNC in the nasal and mouth tissues. With the results, we infer that nasal and mouth tissues may be the first host cells of COVID-2019 infection. In our previous report in medRxiv and a recurrent report in New England Journal of Medicine, the COVID-2019 load tends to be higher in the nasal-swabs than in throat-swabs. We believe the roles of nasal and mouth tissues in COVID-2019 infection should be investigated, and we need to pay more attention to protect nose and mouth from COVID-2019 infection.

    Mutations, Recombination and Insertion in the Evolution of 2019-nCoV

    Authors: Aiping Wu; Peihua Niu; Lulan Wang; Hangyu Zhou; Xiang Zhao; Wenling Wang; Jingfeng Wang; Chengyang Ji; Xiao Ding; Xianyue Wang; Roujian Lu; Sarah Gold; Saba Aliyari; Shilei Zhang; Ellee Vikram; Angela Zou; Emily Lenh; Janet Chen; Fei Ye; Na Han; Yousong Peng; Haitao Guo; Guizhen Wu; Taijiao Jiang; Wenjie Tan; Genhong Cheng

    doi:10.1101/2020.02.29.971101 Date: 2020-03-02 Source: bioRxiv

    BackgroundThe 2019 novel coronavirus (2019-nCoV or SARS-CoV-2) has spread more rapidly than any other betacoronavirus including SARS-CoV MESHD and MERS-CoV. However, the mechanisms responsible for infection and molecular evolution of this virus remained unclear. MethodsWe collected and analyzed 120 genomic sequences of 2019-nCoV including 11 novel genomes from patients in China. Through comprehensive analysis of the available genome sequences of 2019-nCoV strains, we have tracked multiple inheritable SNPs and determined the evolution of 2019-nCoV relative to other coronaviruses. ResultsSystematic analysis of 120 genomic sequences of 2019-nCoV revealed co-circulation of two genetic subgroups with distinct SNPs markers, which can be used to trace the 2019-nCoV spreading pathways to different regions and countries. Although 2019-nCoV, human and bat SARS-CoV share high homologous in overall genome structures, they evolved into two distinct groups with different receptor entry specificities through potential recombination in the receptor binding regions. In addition, 2019-nCoV has a unique four amino acid insertion between S1 and S2 domains of the spike protein PROTEIN, which created a potential furin HGNC or TMPRSS2 HGNC cleavage site. ConclusionsOur studies provided comprehensive insights into the evolution and spread of the 2019-nCoV. Our results provided evidence suggesting that 2019-nCoV may increase its infectivity through the receptor binding domain recombination and a cleavage site insertion. One Sentence SummaryNovel 2019-nCoV sequences revealed the evolution and specificity of betacoronavirus with possible mechanisms of enhanced infectivity.

    The ACE2 HGNC expression of maternal-fetal interface and fetal organs indicates potential risk of vertical transmission of SARS-COV-2

    Authors: Mengmeng Li; Liang Chen; Chenglong Xiong; Xiangjie Li

    doi:10.1101/2020.02.27.967760 Date: 2020-02-27 Source: bioRxiv

    Recent studies have demonstrated that SARS-CoV-2 cell entry depends on both ACE2 HGNC and TMPRSS2 HGNC genes (DOI: 10.1016/j.cell.2020.02.052), but our current work only focus on ACE2 HGNC, which is insufficient to support the conclusion of this paper. So the authors have withdrawn their manuscript whilst they perform additional experiments and analysis to test some of their conclusions further. Therefore, the authors do not wish this work to be cited as reference for the project.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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