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HGNC Genes

SARS-CoV-2 proteins

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    Smoking modulates different secretory subpopulations expressing SARS-CoV-2 entry genes in the nasal and bronchial airways

    Authors: Ke Xu; Xingyi Shi; Chris Husted; Rui Hong; Yichen Wang; Boting Ning; Travis Sullivan; Kimberly M Rieger-Christ; Fenghai Duan; Helga Marques; Adam C Gower; Xiaohui Xiao; Hanqiao Liu; Gang Liu; Grant Duclos; Avrum Spira; Sarah A Mazzilli; Ehab Billatos; Marc E Lenburg; Joshua D Campbell; Jennifer Beane

    doi:10.1101/2021.03.30.21254564 Date: 2021-04-04 Source: medRxiv

    Coronavirus Disease 2019 MESHD ( COVID-19 MESHD) is caused by severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), which infects host cells with help from the Viral Entry (VE) proteins ACE2 HGNC, TMPRSS2 HGNC, and CTSL HGNC. Proposed risk factors for viral infection MESHD, as well as the rate of disease progression, include age, sex, chronic obstructive pulmonary disease MESHD, cancer MESHD, and cigarette smoking. To investigate whether the proposed risk factors increase viral infection MESHD by modulation of the VE genes, we examined gene expression profiles of 796 nasal and 1,673 bronchial samples across four lung cancer MESHD screening cohorts containing individuals without COVID-19 MESHD. Smoking was the only clinical factor reproducibly associated with the expression of any VE gene across cohorts. ACE2 HGNC expression was significantly up-regulated with smoking in the bronchus but significantly down-regulated with smoking in the nose. Furthermore, expression of individual VE genes were not correlated between paired nasal and bronchial samples from the same patients. Single-cell RNA-seq of nasal brushings revealed that an ACE2 HGNC gene module was detected in a variety of nasal secretory cells with the highest expression in the C15orf48 HGNC+ secretory cells, while a TMPRSS2 HGNC gene module was most highly expressed in nasal keratinizing epithelial cells. In contrast, single-cell RNA-seq of bronchial brushings revealed that ACE2 HGNC and TMPRSS2 HGNC gene modules were most enriched in MUC5AC HGNC+ bronchial goblet cells. The CTSL HGNC gene module was highly expressed in immune populations of both nasal and bronchial brushings. Deconvolution of bulk RNA-seq showed that the proportion of MUC5AC HGNC+ goblet cells was increased in current smokers in both the nose and bronchus but proportions of nasal keratinizing epithelial cells, C15orf48 HGNC+ secretory cells, and immune cells were not associated with smoking status. The complex association between VE gene expression and smoking in the nasal and bronchial epithelium revealed by our results may partially explain conflicting reports on the association between smoking and SARS-CoV-2 infection MESHD.

    Antidepressant and antipsychotic drugs reduce viral infection MESHD by SARS-CoV-2 and fluoxetine show antiviral activity against the novel variants in vitro

    Authors: Merve Senem Fred; Suvi Kuivanen; Hasan Ugurlu; Plinio Cabrera Casarotto; Lev Levanov; Kalle Saksela; Olli Vapalahti; Eero Castren

    doi:10.1101/2021.03.22.436379 Date: 2021-03-23 Source: bioRxiv

    Background and Purpose: Repurposing of currently available drugs is a valuable strategy to tackle the consequences of COVID-19 MESHD. Recently, several studies have investigated the effect of psychoactive drugs on SARS-CoV-2 in cell culture models as well as in clinical practice. Our aim was to expand these studies and test some of these compounds against newly emerged variants. Experimental Approach: Several antidepressant drugs and antipsychotic drugs with different primary mechanisms of action were tested in ACE2 HGNC/ TMPRSS2 HGNC-expressing human embryonic kidney cells against the infection by SARS-CoV-2 spike PROTEIN protein-dependent pseudoviruses. Some of these compounds were also tested in human lung epithelial cell line, Calu-1, against the first wave (B.1) lineage of SARS-CoV-2 and the variants of concern, B.1.1.7 and B.1.351. Key Results: Several clinically used antidepressants, including fluoxetine, citalopram, reboxetine, imipramine, as well as antipsychotic compounds chlorpromazine, flupenthixol, and pimozide inhibited the infection by pseudotyped viruses with minimal effects on cell viability. The antiviral action of several of these drugs was verified in Calu-1 cells against the (B.1) lineage of SARS-CoV-2. By contrast, the anticonvulsant carbamazepine, and novel antidepressants ketamine and its derivatives as well as MAO and phosphodiesterase inhibitors phenelzine and rolipram, respectively, showed no activity in the pseudovirus model. Furthermore, fluoxetine remained effective against pseudo viruses with N501Y, K417N, and E484K spike mutations, and the VoC-1 (B.1.1.7) and VoC-2 (B.1.351) variants of SARS-CoV-2. Conclusion and Implications: Our study confirms previous data and extends information on the repurposing of these drugs to counteract SARS-CoV-2 infection MESHD including different variants of concern.

    Impaired local intrinsic immunity to SARS-CoV-2 infection MESHD in severe COVID-19 MESHD

    Authors:

    doi:10.1101/2021.02.20.431155 Date: 2021-02-20 Source: bioRxiv

    Infection with SARS-CoV-2, the virus that causes COVID-19 MESHD, can lead to severe lower respiratory illness MESHD including pneumonia MESHD and acute respiratory distress syndrome MESHD, which can result in profound morbidity and mortality. However, many infected individuals are either asymptomatic or have isolated upper respiratory symptoms, which suggests that the upper airways represent the initial site of viral infection MESHD, and that some individuals are able to largely constrain viral pathology to the nasal and oropharyngeal tissues. Which cell types in the human nasopharynx are the primary targets of SARS-CoV-2 infection MESHD, and how infection influences the cellular organization of the respiratory epithelium remains incompletely understood. Here, we present nasopharyngeal samples from a cohort of 35 individuals with COVID-19 MESHD, representing a wide spectrum of disease states from ambulatory to critically ill, as well as 23 healthy and intubated patients without COVID-19 MESHD. Using standard nasopharyngeal swabs, we collected viable cells and performed single-cell RNA-sequencing (scRNA-seq), simultaneously profiling both host and viral RNA. We find that following infection with SARS-CoV-2, the upper respiratory epithelium undergoes massive reorganization: secretory cells diversify and expand, and mature epithelial cells are preferentially lost. Further, we observe evidence for deuterosomal cell and immature ciliated cell expansion, potentially representing active repopulation of lost ciliated cells through coupled secretory cell differentiation. Epithelial cells from participants with mild/moderate COVID-19 MESHD show extensive induction of genes associated with anti-viral and type I interferon responses. In contrast, cells from participants with severe lower respiratory symptoms appear globally muted in their anti-viral capacity, despite substantially higher local inflammatory myeloid populations and equivalent nasal viral loads. This suggests an essential role for intrinsic, local epithelial immunity in curbing and constraining viral-induced pathology. Using a custom computational pipeline, we characterized cell-associated SARS-CoV-2 RNA and identified rare cells with RNA intermediates strongly suggestive of active replication. Both within and across individuals, we find remarkable diversity and heterogeneity among SARS-CoV-2 RNA+ host cells, including developing/immature and interferon-responsive ciliated cells, KRT13 HGNC+ "hillock"-like cells, and unique subsets of secretory, goblet, and squamous MESHD cells. Finally, SARS-CoV-2 RNA+ cells, as compared to uninfected bystanders, are enriched for genes involved in susceptibility (e.g., CTSL HGNC, TMPRSS2 HGNC) or response (e.g., MX1 HGNC, IFITM3 HGNC, EIF2AK2 HGNC) to infection. Together, this work defines both protective and detrimental host responses to SARS-CoV-2, determines the direct viral targets of infection, and suggests that failed anti-viral epithelial immunity in the nasal mucosa may underlie the progression to severe COVID-19 MESHD.

    Endothelial cells elicit a pro-inflammatory response to SARS-COV-2 without productive viral infection MESHD

    Authors: Lilian Schimmel; Keng Yih Chew; Claudia Stocks; Teodor Yordanov; Tish Essebier; Arutha Kulasinghe; James Monkman; Anna Flavia Ribeiro dos Santos Miggiolaro; Lucia De Noronha; Anne K Lagendijk; Kate Schroder; Larisa Labzin; Emma J Gordon; Kirsty R Short

    doi:10.1101/2021.02.14.431177 Date: 2021-02-16 Source: bioRxiv

    Thrombotic and microvascular complications are frequently seen in deceased COVID-19 MESHD patients, suggesting that vascular pathology is a major driver of severe disease. However, whether this is caused by direct viral infection of the endothelium or inflammation MESHD-induced endothelial activation remains highly contentious. What role the endothelium plays in viral amplification and inflammation MESHD thus remains a key unresolved question in the pathogenesis of SARS-CoV-2. Here, we use patient autopsy samples, primary human endothelial cells and an in vitro model of the pulmonary epithelial-endothelial cell barrier to show that primary human endothelial cells express the SARS-CoV-2 receptor ACE2 HGNC and the protease TMPRSS2 HGNC, albeit at low levels. Accordingly, when present in a sufficiently high concentration, SARS-CoV-2 can enter primary human endothelial cells from either the apical or basolateral surface. Whilst inducing an inflammatory response, this is not a productive infection. We further demonstrate that in a co-culture model of the pulmonary epithelial-endothelial barrier, endothelial cells are not infected with SARS-CoV-2. They do however, sense and respond to an infection in the adjacent epithelial cells, resulting in the induction of a pro-inflammatory response. Taken together, these data suggest that in vivo, endothelial cells are unlikely to be infected with SARSCoV-2 and that infection is only likely to occur if the adjacent pulmonary epithelium is denuded (basolateral infection) or a high viral load is present in the blood (apical infection). In such a scenario, whilst SARS-CoV-2 infection MESHD of the endothelium can occur, it does not contribute to viral amplification. However, endothelial cells are still likely to play a key role in SARS-CoV-2 pathogenesis by sensing and mounting a pro-inflammatory response to SARS-CoV-2.

    COVIDENZA - A Prospective, Multicenter, Randomized PHASE II Clinical Trial of Enzalutamide Treatment to Decrease the Morbidity in Patients with Corona Virus Disease MESHD 2019 ( COVID-19 MESHD)

    Authors: Karin Welen; Anna Överby Wernstedt; Clas Ahlm; Eva Freyhult; David Robinsson; Anna Jonsson Henningsson; Johan Stranne; Daniel Bremell; Martin Angelin; Elisabeth Lindquist; Robert Buckland; Camilla Thellenberg Karlsson; Karlis Pauksens; Anna Bill Axelsson; Olof Akre; Cecilia Ryden; Magnus Wagenius; Anders Bjartell; Anna Nilsson; Johan Styrke; Johanna Repo; Åse Östholm Balkhed; Katarina Niward; Magnus Gisslen; Andreas Josefsson

    doi:10.21203/rs.3.rs-229140/v1 Date: 2021-02-10 Source: ResearchSquare

    ObjectivesThe main goal of the COVIDENZA trial is to evaluate if inhibition of testosterone signalling by enzalutamide can improve the outcome of patients hospitalized for COVID-19 MESHD. The hypothesis is based on the observation that the majority of patients in need of intensive care are male, and the connection between androgen receptor HGNC signalling and expression of TMPRSS2 HGNC, an enzyme important for SARS-CoV-2 host cell internalization.Trial designHospitalized COVID-19 MESHD patients will be randomised (2:1) to enzalutamide plus standard of care vs. standard of care designed to identify superiority.ParticipantsIncluded participants, men or women above 50 years of age, must be hospitalized for PCR confirmed COVID-19 MESHD symptoms and not in need of immediate mechanical ventilation. Major exclusion criteria are breast-feeding or pregnant women, hormonal treatment for prostate or breast cancer MESHD, treatment with immunosuppressive drugs, current symptomatic unstable cardiovascular disease MESHD (see additional file 1 for further details). The trial is registered at Umeå University Hospital, Region Västerbotten, Sweden and 8 hospitals are approved for inclusion in Sweden.Intervention and comparatorPatients randomised to the treatment arm will be treated orally with 160 mg (4x40 mg) enzalutamide (Xtandi®) daily, for five consecutive days. The study is not placebo controlled. The comparator is standard of care treatment for patients hospitalised with COVID-19 MESHD.Main outcomesThe primary endpoints of the study are (time to) need of mechanical ventilation or discharge from hospital as assessed by a clinical 7-point ordinal scale (up to 30 days after inclusion).RandomisationRandomisation was stratified by center and sex. Each strata was randomized separately with block size six with a 2:1 allocation ratio (enzalutamide + “standard of care”: “standard of care”). The randomisation list, with consecutive subject numbers, was generated by an independent statistician using the PROC PLAN procedure of SAS version 9.4 software (SAS Institute, Inc, Cary, North Carolina)Blinding (masking)This is an open-label trial.Numbers to be randomised (sample size)The trial is designed to have three phases. The first, an exploration phase of 45 participants (30 treatment and 15 control) will focus on safety and includes a more extensive laboratory assessment as well as more frequent safety evaluation. The second prolongation phase, includes the first 100 participants followed by an interim analysis to define the power of the study. The third phase is the continuation of the study up to maximum 600 participants included in total.Trial StatusThe current protocol version is COVIDENZA v2.0 as of September 10, 2020. Recruitment started July 29, 2020 and is presently in safety pause after the first exploration phase. Recruitment is anticipated to be complete by 31 December 2021.Trial registrationEudract number 2020-002027-10ClinicalTrials.gov Identifier: NCT04475601, registered June 8, 2020

    Immune response to SARS-CoV-2 in the nasal mucosa in children and adults

    Authors: Clarissa M Koch; Andrew D Prigge; Kishore R Anekalla; Avani Shukla; Hanh Chi Do-Umehara; Leah Setar; Jairo Chavez; Hiam Abdala-Valencia; Yuliya Politanska; Nikolay S Markov; Grant R Hahn; Taylor Heald-Sargent; L Nelson Sanchez-Pinto; William J Muller; Alexander V Misharin; Karen M Ridge; Bria M Coates

    doi:10.1101/2021.01.26.21250269 Date: 2021-01-28 Source: medRxiv

    Rationale: Despite similar viral load and infectivity rates between children and adults infected with SARS-CoV-2, children rarely develop severe illness. Differences in the host response to the virus at the primary infection site are among the proposed mechanisms. Objectives: To investigate the host response to SARS-CoV-2, respiratory syncytial virus (RSV), and influenza virus (IV) in the nasal mucosa in children and adults. Methods: Clinical outcomes and gene expression in the nasal mucosa were analyzed in 36 children hospitalized with SARS-CoV-2 infection MESHD, 24 children with RSV infection MESHD, 9 children with IV infection, 16 adults with mild to moderate SARS-CoV-2 infection MESHD, and 7 healthy pediatric and 13 healthy adult controls. Results: In both children and adults, infection with SARS-CoV-2 leads to an interferon response in the nasal mucosa. The magnitude of the interferon response correlated with the abundance of viral reads and was comparable between symptomatic children and adults infected with SARS-CoV-2 and symptomatic children infected with RSV MESHD and IV. Cell type deconvolution identified an increased abundance of immune cells in the samples from children and adults with a viral infection MESHD. Expression of ACE2 HGNC and TMPRSS2 HGNC - key entry factors for SARS-CoV-2 - did not correlate with age or presence or absence of viral infection MESHD. Conclusions: Our findings support the hypothesis that differences in the immune response to SARS-CoV-2 determine disease severity, independent of viral load and interferon response at the primary infection primary site. Keywords: COVID-19 MESHD, pneumonia MESHD, viral infections MESHD, interferons

    Dodging COVID-19 MESHD Infection: Low Expression and Localization of ACE2 HGNC and TMPRSS2 HGNC in Human Umbilical Cord-Derived Mesenchymal Stem Cells

    Authors: Jonathan J Hernandez; Doyle E Beaty; Logan L Fruhwirth; Ana P Lopes Chaves; Neil H Riordan

    doi:10.21203/rs.3.rs-154351/v1 Date: 2021-01-25 Source: ResearchSquare

    BackgroundMesenchymal stem cells derived from human umbilical cord (hUC-MSCs) have immunomodulatory properties that are of interest to treat novel coronavirus disease 2019 MESHD ( COVID-19 MESHD). Leng et al. recently reported that hUC-MSCs derived from one donor negatively expressed Angiotensin-Converting Enzyme 2 HGNC ( ACE2 HGNC), a key protein for viral infection MESHD along with Transmembrane Serine Protease 2 ( TMPRSS2 HGNC). MethodsExpression of ACE2 HGNC and TMPRSS2 HGNC was analyzed in 24 lots of hUC-MSCs derived fromWharton's jelly via quantitative polymerase chain reaction (qPCR), Western Blot, immunofluorescence and flow cytometry using 24 different donors. ResultshUC-MSCs had significantly lower ACE2 HGNC (p=0.002) and TMPRSS2 HGNC (p=0.008) expression compared with human lung tissue homogenates in Western blot analyses. Little to no expression of ACE2 HGNC was observed in hUC-MSC by qPCR, and they were not observable with immunofluorescence in hUC-MSCs cell membranes. A negative ACE2 HGNC and TMPRSS2 HGNC population percentage of 95.3% ±15.55 was obtained for hUC-MSCs via flow cytometry, with only 4.6% ACE2 HGNC and 29.5% TMPRSS2 HGNC observable positive populations. ConclusionsWe have demonstrated negative expression of ACE2 HGNC and low expression of TMPRSS2 HGNC in 24 lots of hUC-MSCs. This has crucial implications for the design of future therapeutic options for COVID-19 MESHD, since hUC-MSCs would have the ability to “dodge” viral infection to exert their immunomodulatory effects.

    Comparative Study of Epithelial Entry Gene Expression of SARS-Cov-2 and Other Human Viral Species in Asthma: Differences by Sex, Airway Location Aand Disease MESHD Endotype

    Authors: Mackenzie Coden; Lucas Loffredo; Hiam Abdala-Valencia; Sergejs Berdnikovs

    id:10.20944/preprints202101.0266.v1 Date: 2021-01-14 Source: Preprints.org

    Epithelial characteristics underlying the differential susceptibility of chronic asthma to SARS-CoV-2 MESHD ( COVID-19 MESHD) and other viral infections MESHD are currently unclear. By revisiting transcriptomic data from patients with Th2 low versus Th2 high asthma, as well as mild, moderate and severe asthmatics, we characterized the changes in expression of human coronavirus and influenza viral entry genes relative to sex, airway location and disease endotype. We found sexual dimorphism in expression of COVID-19 MESHD genes ACE2, TMPRSS2 HGNC, TMPRSS4 HGNC, and SLC6A19 HGNC. ACE2 receptor downregulation occurred specifically in females in Th2 high asthma, while proteases broadly assisting coronavirus and influenza viral entry, TMPRSS2 HGNC and TMPRSS4 HGNC, were highly upregulated in both sexes. Overall, changes in COVID-19 MESHD gene expression were specific to Th2 high molecular endotype of asthma MESHD, and different by asthma severity and airway location. The downregulation of ACE2 ( COVID-19 MESHD, SARS) and ANPEP (HCoV-229E) viral receptors correlated with loss of club and ciliated cells in Th2 high asthma, while the increase in DPP4 (MERS-CoV), ST3GAL4, and ST6GAL1 (influenza) associated with an increase in goblet and basal activated cells. Overall, this study elucidates sex, airway location, disease endotype and changes in epithelial heterogeneity as factors underlying asthmatic susceptibility, or lack thereof, to COVID-19 MESHD.

    The Contrasting Role of Nasopharyngeal Angiotensin Converting Enzyme 2 HGNC ( ACE2 HGNC) Expression in SARS-CoV-2 Infection MESHD: A Cross-Sectional Study of People Tested for COVID-19 MESHD in British Columbia

    Authors: Aidan M Nikiforuk; Kevin S Kuchinski; David D W Twa; Christine D Lukac; Hind Sbihi; C Andrew Basham; Christian Steidl; Natalie A Prystajecky; Agatha N Jassem; Mel Krajden; David M Patrick; Inna Sekirov

    doi:10.1101/2020.11.23.20237206 Date: 2020-11-24 Source: medRxiv

    Summary Background Angiotensin converting enzyme 2 HGNC ( ACE2 HGNC) serves as the host receptor for SARS-CoV-2, with a critical role in viral infection MESHD. We aim to understand population level variation of nasopharyngeal ACE2 HGNC expression in people tested for COVID-19 MESHD and the relationship between ACE2 HGNC expression and SARS-CoV-2 viral RNA load, while adjusting for expression of the complementary protease, Transmembrane serine protease 2 ( TMPRSS2 HGNC), soluble ACE2 HGNC, age, and biological sex. Methods A cross-sectional study of n=424 participants aged 1-104 years referred for COVID-19 MESHD testing was performed in British Columbia, Canada. Participants who tested negative or positive for COVID-19 MESHD were matched by age and biological sex. Viral and host gene expression was measured by quantitative reverse-transcriptase polymerase chain reaction. Bivariate analysis and multiple linear regression were performed to understand the role of nasopharyngeal ACE2 HGNC expression in SARS-CoV-2 infection MESHD. The ACE2 HGNC gene was targeted to measure expression of transmembrane and soluble transcripts. Findings Analysis shows no association between age and nasopharyngeal ACE2 HGNC expression in those who tested negative for COVID-19 MESHD (P=0[middot]092). Mean expression of transmembrane (P=1[middot]2e-4), soluble ACE2 HGNC (P<0[middot]0001) and TMPRSS2 HGNC (P<0[middot]0001) differed between COVID-19 MESHD-negative and -positive groups. In bivariate analysis of COVID-19 MESHD-positive participants, expression of transmembrane ACE2 HGNC positively correlated with SARS-CoV-2 RNA viral load (P<0[middot]0001), expression of soluble ACE2 HGNC negatively correlated (P<0[middot]0001), and no correlation was found with TMPRSS2 HGNC (P=0[middot]694). Multivariable analysis showed that the greatest viral RNA loads were observed in participants with high transmembrane ACE2 HGNC expression (B=0[middot]886, 95%CI:[0[middot]596 to 1[middot]18]), while expression of soluble ACE2 HGNC may protect against high viral RNA load in the upper respiratory tract (B= -0[middot]0990, 95%CI:[-0[middot]176 to -0[middot]0224]). Interpretation Nasopharyngeal ACE2 HGNC expression plays a dual, contrasting role in SARS-CoV-2 infection MESHD of the upper respiratory tract. Transmembrane ACE2 HGNC positively correlates, while soluble ACE2 HGNC negatively correlates with viral RNA load after adjusting for age, biological sex and expression of TMPRSS2 HGNC. Funding This project (COV-55) was funded by Genome British Columbia as part of their COVID-19 MESHD rapid response initiative.

    SARS-CoV-2 and Malayan pangolin coronavirus infect human endoderm, ectoderm and induced lung progenitor cells

    Authors: Kuanhui Xiang; Bixia Hong; Xinyuan Lai; Yangzhen Chen; Tianming Luo; Xiaoping An; Lihua Song; Hui Zhuang; Huahao Fan; Tong Li; Yi-Gang Tong; Maria Florencia Gomez Castro; Yongxiang Zhao; Hinissan Pascaline Kohio; Gaopeng Hou; Baochao Fan; Beibei Niu; Rongli Guo; Paul W. Rothlauf; Adam L. Bailey; Xin Wang; Pei-Yong Shi; Sean P. J. Whelan; Michael S. Diamond; Adrianus C.M. Boon; Bin Li; Siyuan Ding; John S Pauk; Scott D. Boyd; James R. Heath

    doi:10.1101/2020.09.25.313270 Date: 2020-09-25 Source: bioRxiv

    Since the infection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in several somatic cells, little is known about the infection of SASRS-CoV-2 and its related pangolin coronavirus (GX_P2V). Here we present for the first time that SARS-CoV-2 pseudovirus and GX_P2V could infect lung MESHD progenitor and even anterior foregut endoderm cells causing these cells death MESHD, which differentiated from human embryonic stem cells (hESCs). The infection and replication of SARS-CoV-2 and GX_P2V were inhibited when treated with whey protein of breastmilk and Remdesivir, confirming that these two viruses could infect lung MESHD progenitor and even anterior foregut endoderm. Moreover, we found that SARS-CoV-2 pseudovirus could infect endoderm and ectoderm. We found that whey protein blocked SARS-CoV-2 infecting these cells. In line with the SARS-CoV-2 results, GX_P2V could also infected endoderm and ectoderm, and also was inhibited by Remdesivir treatment. Although expressing coronavirus related receptor such as ACE2 HGNC and TMPRSS2 HGNC, mesoderm cells are not permissive for SARS-CoV-2 and GX_P2V infection, which needed further to study the mechanisms. Interestingly, we also found that hESCs, which also express ACE2 HGNC and TMPRSS2 HGNC markers, are permissive for GX_P2V but not SARS-CoV-2 pseudovirus infection MESHD and replication, indicating the widespread cell types for GX_P2V infection. Heparin treatment blocked efficiently viral infection MESHD. These results provided insight that these stem cells maybe provided a stable repository of coronavirus function or genome. The potential consequence of SARS-CoV-2 and animal coronavirus such as GX_P2V infection in hESCs, germ layer and induced progenitors should be closely monitored.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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