Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (11)

ProteinN (1)

ProteinE (1)


SARS-CoV-2 Proteins
    displaying 1 - 10 records in total 22
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    Genome-wide CRISPR activation screen identifies novel receptors for SARS-CoV-2 entry MESHD

    Authors: Shiyou Zhu; Ying Liu; Zhuo Zhou; Zhiying Zhang; Xia Xiao; Zhiheng Liu; Ang Chen; Xiaojing Dong; Feng Tian; Shihua Chen; Yiyuan Xu; Chunhui Wang; Qiheng Li; Xuran Niu; Qian Pan; Shuo Du; Junyu Xiao; Jianwei Wang; Wensheng Wei

    doi:10.1101/2021.04.08.438924 Date: 2021-04-09 Source: bioRxiv

    The ongoing pandemic of coronavirus disease 2019 MESHD ( COVID-19 MESHD) caused by severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2) has been endangering worldwide public health and economy. SARS-CoV-2 infects MESHD a variety of tissues where the known receptor ACE2 HGNC is low or almost absent, suggesting the existence of alternative pathways for virus entry. Here, we performed a genome-wide barcoded-CRISPRa screen to identify novel host factors that enable SARS-CoV-2 infection MESHD. In addition to known host proteins, i.e PROTEIN. ACE2 HGNC, TMPRSS2 HGNC, and NRP1 HGNC, we identified multiple host components, among which LDLRAD3 HGNC, TMEM30A HGNC, and CLEC4G HGNC were confirmed as functional receptors for SARS-CoV-2. All these membrane proteins bind directly to spike's N-terminal domain ( NTD HGNC). Their essential and physiological roles have all been confirmed in either neuron or liver cells. In particular, LDLRAD3 HGNC and CLEC4G HGNC mediate SARS-CoV-2 entry MESHD and infection in a fashion independent of ACE2 HGNC. The identification of the novel receptors and entry mechanisms could advance our understanding of the multiorgan tropism of SARS-CoV-2, and may shed light on the development of the therapeutic countermeasures against COVID-19 MESHD.

    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.

    Comprehensive evaluation of ACE2 HGNC expression in female ovary by single-cell RNA-seq analysis

    Authors: Siming Kong; Zhiqiang Yan; Peng Yuan; Xixi Liu; Yidong Chen; Ming Yang; Wei Chen; Shi Song; Jie Yan; Liying Yan; Jie Qiao

    doi:10.1101/2021.02.23.432460 Date: 2021-02-23 Source: bioRxiv

    Pneumonia induced by severe acute respiratory coronavirus MESHD 2 (SARS-CoV-2) via ACE2 HGNC receptor may affect many organ systems like lung, heart and kidney. An autopsy report revealed positive SARS-Cov-2 detection results in ovary MESHD, however, the developmental-stage-specific and cell-type-specific risk in fetal primordial germ cells (PGCs) and adult women ovary remained unclear. In this study, we used single-cell RNA-sequencing (scRNA-seq) datasets spanning several developmental stages of ovary MESHD including PGCs and cumulus-oocyte complex (COC) to investigate the potential risk of SARS-CoV-2 infection MESHD. We found that PGCs and COC exhibited high ACE2 HGNC expression. More importantly, the ratio of ACE2 HGNC-positive cells was sharply up-regulated in primary stage and ACE2 HGNC was expressed in all oocytes and cumulus cells in preovulatory stage, suggesting the possible risk of SARS-CoV-2 infection MESHD in follicular development. CatB HGNC/L, not TMPRSS2 HGNC, was identified to prime for SARS-CoV-2 entry MESHD in follicle. Our findings provided insights into the potential risk of SARS-CoV-2 infection MESHD during folliculogenesis in adulthood and the possible risk in fetal PGCs.

    Renin HGNC-Angiotensin System Blockade Influences ACE2 HGNC in Human Type II Pneumocytes

    Authors: Mauro G Silva; Nora L Falcoff; Gerardo C Corradi; José Alfie; Rolando F. Seguel; Gabriela Tabaj; Laura Iglesias; Myriam Nuñez; Gabriela R. Guman; Mariela M. Gironacci

    doi:10.21203/ Date: 2021-01-27 Source: ResearchSquare

    Rationale— Angiotensin converting enzyme (ACE) 2 HGNC and the transmembrane protease serine 2 HGNC ( TMPRSS2 HGNC) are key for cellular entry of the type 2 coronavirus that causes severe acute respiratory syndrome MESHD (SARS-CoV2), the etiological agent of coronavirus-19 disease MESHD ( COVID-19 MESHD). There has been a growing concern that renin HGNC-angiotensin system (RAS) blockade with ACE HGNC inhibitors (ACEIs) or type 1 angiotensin (Ang II) receptor blockers (ARBs) increases ACE2 HGNC expression and then elevate patient susceptibility to SARS-CoV-2.  However, evidence about RAS blockade and ACE2 HGNC in human lung are lacking.Objective– To investigate RAS blockade on ACE2 HGNC and TMPRSS2 HGNC in type II pneumocytes of human lung parenchymal of untreated and ACEI/ARB-treated hypertensive MESHD subjects.Methods and Results– ACE2 HGNC and TMPRSS2 HGNC protein expression were measured by immunohistochemistry. We found that smoking and RAS blockade influence on the percentage of human ACE2 HGNC-expressing type II pneumocytes (p= 0.026). Smokers subjects under RAS blockade treatment exhibited higher percentage of ACE2 HGNC-expressing type II pneumocytes than normotensive ones. Within the ACEI/ARB-treated group, the percentage of ACE2 HGNC-expressing type II pneumocytes was higher in smokers than never smokers. A significant association between ACE2 HGNC immunostaining intensity and smoking on subjects over 60 years old was found (p= 0.05): older smokers exhibited higher ACE2 HGNC protein levels compared to youngers. The percentage of TMPRSS2 HGNC-expressing type II pneumocytes was greater in men than women (p= 0.026) and in subjects under 60 years old (p= 0.040) and trend to be higher in ACEI/ARB-treated subjects than normotensives (p= 0.060). A significant association between TMPRSS2 HGNC immunostaining intensity with smoking and age or with RAS blockade MESHD and age or with RAS blockade MESHD and smoking was observed. Older or smokers subjects under ACEI/ARB treatment exhibited higher TMPRSS2 HGNC protein levels than youngers or never smokers.Conclusions— ACE2 HGNC and TMPRSS2 HGNC are influenced by smoking and ACEI/ARB treatment. These findings help explain the increased susceptibility to COVID-19 MESHD in subjects with treated cardiovascular-related pathologies. 

    Enzalutamide, a prostate cancer MESHD therapeutic, downregulates TMPRSS2 HGNC in lung and reduces cellular entry of SARS-CoV-2

    Authors: D. A. Leach; A. Mohr; E. S. Giotis; A. M. Isac; L. L. Yates; W. S. Barclay; R. M. Zwacka; C. L. Bevan; G. N. Brooke

    doi:10.21203/ Date: 2020-12-29 Source: ResearchSquare

    The COVID-19 pandemic MESHD, caused by the novel human coronavirus SARS-CoV-2 coronavirus MESHD, attacks various organs but most destructively the lung. It has been shown that SARS-CoV-2 entry into lung cells requires two host cell surface proteins: ACE2 HGNC and TMPRSS2 HGNC. Downregulation of one or both of these is thus a potential therapeutic approach for COVID-19 MESHD TMPRSS2 HGNC is a known target of the androgen receptor HGNC, a ligand-activated transcription factor; activation of the androgen receptor HGNC increases TMPRSS2 HGNC levels in various tissues, most notably the prostate. We show here that treatment with the antiandrogen enzalutamide – a well-tolerated drug widely used in advanced prostate cancer MESHD – reduces TMPRSS2 HGNC levels in human lung cells. Further, enzalutamide treatment of mice dramatically decreased Tmprss2 levels in the lung. To determine therapeutic potential, we assessed uptake of SARS-CoV-2 Spike MESHD SARS-CoV-2 Spike PROTEIN protein pseudotyped lentivirus and live SARS-CoV-2 into human lung cells and saw a significant reduction in viral entry and infection upon treatment with the antiandrogens enzalutamide and bicalutamide. In support of this new experimental data, analysis of existing datasets shows striking co-expression of AR and TMPRSS2 HGNC, including in specific lung cell types that are targeted by SARS-CoV-2. Together, the data presented provides strong evidence to support clinical trials to assess the efficacy of antiandrogens as a treatment option for COVID-19 MESHD.

    Paradoxical effects of cigarette smoke and COPD MESHD on SARS-CoV2 infection MESHD and disease

    Authors: Michael Tomchaney; Marco Contoli; Jonathan Mayo; Simonetta Baraldo; Shuaizhi Li; Carly Cabel; David Bull; Scott Lick; Joshua Malo; Steve Knoper; Samuel Kim; Judy Tram; Joselyn Rojas Quintero; Monica Kraft; Julie Ledford; Fernando D Martinez; Curtis Thorne; Farrah Kheradmand; Samuel K Campos; Alberto Papi; Francesca Polverino

    doi:10.1101/2020.12.07.413252 Date: 2020-12-07 Source: bioRxiv

    IntroductionHow cigarette smoke (CS) and chronic obstructive pulmonary disease MESHD ( COPD MESHD) affect severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection MESHD and severity is controversial. We investigated the protein and mRNA expression of SARS-CoV-2 entry receptor ACE2 HGNC and proteinase TMPRSS2 HGNC in lungs from COPD MESHD patients and controls, and lung tissue from mice exposed acutely and chronically to CS. Also, we investigated the effects of CS exposure on SARS-CoV-2 infection MESHD in human bronchial epithelial cells. MethodsIn Cohort 1, ACE2 HGNC-positive cells were quantified by immunostaining in FFPE sections from both central and peripheral airways. In Cohort 2, we quantified pulmonary ACE2 HGNC protein levels by immunostaining and ELISA, and both ACE2 HGNC and TMPRSS2 HGNC mRNA levels by RT-qPCR. In C57BL/6 WT mice exposed to air or CS for up to 6 months, pulmonary ACE2 protein levels were quantified by triple immunofluorescence staining and ELISA. The effects of CS exposure on SARS-CoV-2 infection MESHD were evaluated after 72hr in vitro infection of Calu-3 cells. After SARS-CoV-2 infection MESHD, the cells were fixed for IF staining with dsRNA-specific J2 monoclonal Ab, and cell lysates were harvested for WB of viral nucleocapsid (N) protein PROTEIN. Supernatants (SN) and cytoplasmic lysates were obtained to measure ACE2 HGNC levels by ELISA. ResultsIn both human cohorts, ACE2 HGNC protein and mRNA levels were decreased in peripheral airways from COPD MESHD patients versus both smoker and NS controls, but similar in central airways. TMPRSS2 HGNC levels were similar across groups. Mice exposed to CS had decreased ACE2 protein levels in their bronchial and alveolar epithelia MESHD versus air-exposed mice exposed to 3 and 6 months of CS. In Calu3 cells in vitro, CS-treatment abrogated infection to levels below the limit of detection. Similar results were seen with WB for viral N protein PROTEIN, showing peak viral protein synthesis at 72hr. ConclusionsACE2 levels were decreased in both bronchial and alveolar epithelial MESHD cells from uninfected COPD MESHD patients versus controls, and from CS-exposed versus air-exposed mice. CS-pre-treatment did not affect ACE2 levels but potently inhibited SARS-CoV-2 replication in this in vitro model. These findings urge to further investigate the controversial effects of CS and COPD MESHD on SARS-CoV2 infection MESHD.

    SARS-CoV-2 infects cells of the human exocrine and endocrine pancreas and interferes with beta-cell function

    Authors: Janis A. Müller; Rüdiger Groß; Carina Conzelmann; Jana Krüger; Lennart Koepke; Johannes Steinhart; Tatjana Weil; Caterina Prelli Bozzo; Clarissa Read; Giorgio Fois; Tim Eiseler; Julia Gehrmann; Joanne van Vuuren; Isabel M. Wessbecher; Manfred Frick; Ivan G. Costa; Markus Breunig; Michael Schuster; Stefan Liebau; Thomas Seufferlein; Steffen Stenger; Albrecht Stenzinger; Patrick E. MacDonald; Frank Kirchhoff; Konstantin M. J. Sparrer; Paul Walther; Heiko Lickert; Thomas F.E. Barth; Martin Wagner; Jan Münch; Sandra Heller; Alexander Kleger

    doi:10.21203/ Date: 2020-10-21 Source: ResearchSquare

    Preexisting diabetes increases MESHD the risk of a severe course of the pandemic coronavirus disease MESHD coronavirus disease 2019 MESHD ( COVID-19 MESHD). Vice versa, exacerbations of a preexisting diabetes MESHD as well as new-onset diabetes MESHD have been reported upon SARS-CoV-2 infection MESHD. Thus, there is an imperative need to clarify whether human pancreatic endocrine MESHD cells organized within an islet of Langerhans are permissive for and affected by SARS-CoV-2 infection MESHD, and to elucidate the mechanisms underlying the development of diabetes MESHD upon COVID-19 MESHD. Here, we (i) defined ACE2 HGNC and TMPRSS2 HGNC expression patterns in human pancreatic endocrine MESHD and exocrine cell types, (ii) employed human pancreatic MESHD islet cultures to demonstrate susceptibility to SARS-CoV-2 infection MESHD and to viral replication in β-cells, (iii) showed that SARS-CoV-2 attenuates glucose-stimulated insulin HGNC secretion, and (iv) tested remdesivir as eventually effective to prevent β-cell failure. In addition, we (v) visualized viral particles replicating in endocrine pancreatic MESHD cells and define their subcellular localization patterns via transmission electron microscopy, and finally (vi) present examples of cell type specific pancreatic infection MESHD patterns of COVID-19 MESHD deceased patients. Overall, our data demonstrate that SARS-CoV-2 can infect both the exocrine and endocrine compartments of the pancreas MESHD and can perturb β-cell integrity, which might lead to an increased risk for diabetes MESHD.

    Host range projection of SARS-CoV-2: South Asia perspective

    Authors: Rasel Ahmed; Rajnee Hasan; AMAM Zonaed Siddiki; Md. Shahidul Islam; Dallas Nygard; Iryna Abramchuk; Yun-En Chung; Steffany A. L. Bennett; Mathieu Lavallee-Adam; Raul Y. Sanchez-David; Maia Kavanagh Williamson; Jack A. Hassard; Ecco Staller; Brian Hanley; Michael Osborn; Andrew D. Davidson; Wendy S. Barclay; Mohammad Mohiuddin; Naznin Sultana; Kakon Nag; Emily D Crawford; Andreas S Puschnik; Maira Phelps; Amy Kistler; Joseph L DeRisi; Jennifer A Doudna; Daniel A Fletcher; Melanie Ott

    doi:10.1101/2020.09.30.320242 Date: 2020-09-30 Source: bioRxiv

    Severe Acute Respiratory Syndrome Coronavirus 2 MESHD (SARS-CoV-2), the causing agent of Coronavirus Disease MESHD-2019 ( COVID-19 MESHD), is likely to be originated from bat and transmitted through intermediate hosts. However, the immediate source species of SARS-CoV-2 has not yet been confirmed. Here, we used diversity analysis of the angiotensin I converting enzyme 2 HGNC ( ACE2 HGNC) that serves as cellular receptor for SARS-CoV-2 and transmembrane protease serine 2 HGNC ( TMPRSS2 HGNC), which has been proved to be utilized by SARS-CoV-2 for spike PROTEIN protein priming. We also simulated the structure of receptor-binding domain of SARS-CoV-2 spike MESHD SARS-CoV-2 spike PROTEIN protein ( SARS-CoV-2 S RBD MESHD) with the ACE2 HGNCs to investigate their binding affinity to determine the potential intermediate animal hosts that could spread the SARS-CoV-2 virus to humans in South Asia. We identified cow, buffalo, goat and sheep, which are predominant species in the household farming system in South Asia that can potentially be infected by SARS-CoV-2. All the bird species studied along with rat and mouse were considered less potential to interact with SARS-CoV-2. The interaction interfaces of SARS-CoV-2 S RBD MESHD and ACE2 protein complex suggests pangolin as a potential intermediate host in SARS-CoV-2. Our results provide a valuable resource for the identification of potential hosts for SARS-CoV-2 in South Asia and henceforth reduce the opportunity for a future outbreak of COVID-19 MESHD.

    Determinants of SARS-CoV-2 receptor gene expression in upper and lower airways

    Authors: Hananeh Aliee; Florian Massip; Cancan Qi; Maria Stella de Biase; Johannes L van Nijnatten; Elin T.G. Kersten; Nazanin Z. Kermani; Basil Khuder; Judith M Vonk; Roel C H Vermeulen; - U-BIOPRED study group; - Cambridge Lung Cancer Early Detection Programme; - INER-Ciencias Mexican Lung Program; - NHLBI LungMAP Consortium; Margaret Neighbors; Gaik W. Tew; Michele Grimbaldeston; Nick H.T. ten Hacken; Sile Hu; Yike Guo; Xiaoyu Zhang; Kai Sun; Pieter S. Hiemstra; Bruce A. Ponder; Mika J Makela; Kristiina Malmstrom; Robert C. Rintoul; Paul A. Reyfman; Fabian J. Theis; Corry-A Brandsma; Ian Adcock; Wim Timens; Cheng J. Xu; Maarten van den Berge; Roland F. Schwarz; Gerard H. Koppelman; Martijn C. Nawijn; Alen Faiz

    doi:10.1101/2020.08.31.20169946 Date: 2020-09-02 Source: medRxiv

    The recent outbreak of the severe acute respiratory syndrome coronavirus-2 MESHD (SARS-CoV-2), which causes coronavirus disease 2019 MESHD ( COVID-19 MESHD), has led to a worldwide pandemic. One week after initial symptoms develop, a subset of patients progresses to severe disease, with high mortality and limited treatment options. To design novel interventions aimed at preventing spread of the virus and reducing progression to severe disease, detailed knowledge of the cell types and regulating factors driving cellular entry is urgently needed. Here we assess the expression patterns in genes required for COVID-19 MESHD entry into cells and replication, and their regulation by genetic, epigenetic and environmental factors, throughout the respiratory tract using samples collected from the upper (nasal) and lower airways (bronchi). Matched samples from the upper and lower airways show a clear increased expression of these genes in the nose compared to the bronchi and parenchyma. Cellular deconvolution indicates a clear association of these genes with the proportion of secretory epithelial cells. Smoking status was found to increase the majority of COVID-19 MESHD related genes including ACE2 HGNC and TMPRSS2 HGNC but only in the lower airways, which was associated with a significant increase in the predicted proportion of goblet cells in bronchial samples of current smokers. Both acute and second hand smoke were found to increase ACE2 HGNC expression in the bronchus. Inhaled corticosteroids decrease ACE2 HGNC expression in the lower airways. No significant effect of genetics on ACE2 HGNC expression was observed, but a strong association of DNA- methylation with ACE2 HGNC and TMPRSS2 HGNC- mRNA expression was identified in the bronchus.

    Modeling COVID-19 MESHD with Human Pluripotent Stem Cell-Derived Cells Reveals Synergistic Effects of Anti-inflammatory Macrophages with ACE2 HGNC Inhibition Against SARS-CoV-2

    Authors: Fuyu Duan; Liyan Guo; Liuliu Yang; Yuling Han; Abhimanyu Thakur; Benjamin E. Nilsson-Payant; Pengfei Wang; Zhao Zhang; Chui Yan Ma; Xiaoya Zhou; Teng Han; Tuo Zhang; Xing Wang; Dong Xu; Xiaohua Duan; Jenny Xiang; Hung-fat Tse; Can Liao; Weiren Luo; Fang-Ping Huang; Ya-Wen Chen; Todd Evans; Robert E. Schwartz; Benjamin tenOever; David D. Ho; Shuibing Chen; Jie Na; Qizhou Lian; Huanhuan Joyce Chen

    doi:10.21203/ Date: 2020-08-20 Source: ResearchSquare

    Dysfunctional immune responses contribute critically to the progression of Coronavirus Disease MESHD-2019 ( COVID-19 MESHD) from mild to severe stages including fatality, with pro-inflammatory macrophages as one of the main mediators of lung hyper-inflammation MESHD. Therefore, there is an urgent need to better understand the interactions among SARS-CoV-2 permissive cells, macrophage, and the SARS-CoV-2 virus, thereby offering important insights into new therapeutic strategies.  Here, we used directed differentiation of human pluripotent stem cells (hPSCs) to establish a lung and macrophage co-culture system and model the host-pathogen interaction and immune response caused by SARS-CoV-2 infection MESHD. Among the hPSC-derived lung cells, alveolar type II MESHD and ciliated cells are the major cell populations expressing the viral receptor ACE2 HGNC and co-effector TMPRSS2 HGNC, and both were highly permissive to viral infection MESHD. We found that alternatively polarized macrophages (M2) and classically polarized macrophages (M1) had similar inhibitory effects on SARS-CoV-2 infection MESHD. However, only M1 macrophages significantly up-regulated inflammatory factors including IL-6 HGNC and IL-18 HGNC, inhibiting growth and enhancing apoptosis of lung cells. Inhibiting viral entry into target cells using an ACE2 HGNC blocking antibody enhanced the activity of M2 macrophages, resulting in nearly complete clearance of virus and protection of lung cells. These results suggest a potential therapeutic strategy, in that by blocking viral entrance to target cells while boosting anti-inflammatory action of macrophages at an early stage of infection, M2 macrophages can eliminate SARS-CoV-2, while sparing lung cells and suppressing the dysfunctional hyper MESHD-inflammatory response mediated by M1 macrophages.    

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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