Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (99)

ProteinN (5)

ProteinE (3)

NSP5 (2)

ComplexRdRp (1)


SARS-CoV-2 Proteins
    displaying 41 - 50 records in total 240
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    SPINT2 HGNC controls SARS-CoV-2 viral infection and is associated to disease severity

    Authors: Carlos Ramirez; Ashwini Kumar Sharma; Carmon Kee; Leonie Thomas; Steeve Boulant; Carl Herrmann; Victoria A Avanzato; Jonathan E Schulz; Neeltje van Doremalen; Chad Clancy; Vincent Munster; Elisa Casa; Inesa Hyseni; Linda Benincasa; Emanuele Montomoli; Rommie E. Amaro; Jason S McLellan; Rino Rappuoli; Michael Diamond

    doi:10.1101/2020.12.28.424029 Date: 2020-12-28 Source: bioRxiv

    COVID-19 MESHD outbreak is the biggest threat to human health in recent history. Currently, there are over 1.5 million related deaths MESHD and 75 million people infected around the world (as of 22/12/2020). The identification of virulence factors which determine disease susceptibility and severity in different cell types remains an essential challenge. The serine protease TMPRSS2 HGNC has been shown to be important for S protein PROTEIN priming and viral entry, however, little is known about its regulation. SPINT2 HGNC is a member of the family of Kunitz type serine protease inhibitors and has been shown to inhibit TMPRSS2 HGNC. Here, we explored the existence of a co-regulation between SPINT2 HGNC/ TMPRSS2 HGNC and found a tightly regulated protease/inhibitor expression balance across tissues. We found that SPINT2 HGNC negatively correlates with SARS-CoV-2 expression in Calu-3 and Caco-2 cell lines and was down-regulated in secretory cells from COVID-19 MESHD patients. We validated our findings using Calu-3 cell lines and observed a strong increase in viral load after SPINT2 HGNC knockdown. Additionally, we evaluated the expression of SPINT2 HGNC in datasets from comorbid diseases using bulk and scRNA-seq data. We observed its down-regulation in colon, kidney and liver tumors MESHD as well as in alpha pancreatic islets cells from diabetes Type 2 MESHD patients, which could have implications for the observed comorbidities in COVID-19 MESHD patients suffering from chronic diseases MESHD.

    Establishment of a well-characterized SARS-CoV-2 lentiviral pseudovirus neutralization assay using 293T cells with stable expression of ACE2 HGNC and TMPRSS2

    Authors: Sabari Nath Neerukonda; Russell Vassell; Rachel Herrup; Shufeng Liu; Tony Wang; Kazuyo Takeda; Ye Yang; Tsai-Lien Lin; Wei Wang; Carol D. Weiss

    doi:10.1101/2020.12.26.424442 Date: 2020-12-26 Source: bioRxiv

    Pseudoviruses are useful surrogates for highly pathogenic viruses because of their safety, genetic stability, and scalability for screening assays. Many different pseudovirus platforms exist, each with different advantages and limitations. Here we report our efforts to optimize and characterize an HIV-based lentiviral pseudovirus assay for screening neutralizing antibodies for SARS-CoV-2 using a stable 293T cell line expressing human angiotensin converting enzyme 2 HGNC ( ACE2 HGNC) and transmembrane serine protease 2 ( TMPRSS2 HGNC). We assessed different target cells, established conditions that generate readouts over at least a two-log range, and confirmed consistent neutralization titers over a range of pseudovirus input. Using reference sera and plasma panels, we evaluated assay precision and showed that our neutralization titers correlate well with results reported in other assays. Overall, our lentiviral assay is relatively simple, scalable, and suitable for a variety of SARS-CoV-2 entry MESHD and neutralization screening assays.

    Dutasteride Reduces Viral Shedding, Inflammatory Responses and Time-to-Remission in COVID-19 MESHD: Biochemical Findings of a Randomized Double-Blind Placebo Controlled Interventional Trial (DUTA AndroCoV-Trial - Biochemical). 

    Authors: Flávio Adsuara Cadegiani; John McCoy; Carlos Gustavo Wambier; Andy Goren

    doi:10.21203/ Date: 2020-12-24 Source: ResearchSquare

    Importance: SARS-CoV-2 cell entry and infectivity is indirectly dependent on androgenic status and phenotype through the regulation of t ransmembrane protease serine 2 HGNC(T MPRSS2) HGNC, an androgen-mediated proteolytic enzyme that facilitates SARS-CoV-2 entry.  Males, particularly those affected by androgenetic alopecia (AGA) are overrepresented in severe COVID-19 MESHD, while the use of 5-alpha-reductase inhibitors (5ARis), an antiandrogenic drug class, may reduce COVID-19 MESHD severity. Objective: Our objective was to determine if dutasteride, a wide and potent 5ARi, would bring biochemical and virological benefits in early COVID-19 MESHD.Design, Setting, and Participants: A double-blinded, randomized, prospective, investigational study of dutasteride for the treatment of COVID-19 MESHD, as add-on therapy to the local standard of care, for mild or moderate, non-hospitalized subjects confirmed for S ARS-CoV-2 MESHD(The Duta AndroCoV Trial).Interventions:  Dutasteride 0.5mg/day or placebo for 30 days or until full COVID-19 MESHD remission. Nitazoxanide was given 500mg twice a day for six days and azithromycin was given 500mg/day for five days for all subjects.Main Outcome(s) and Measure(s): Remission times for fatigue, ageusia, anosmia, and overall disease, oxygen saturation (%), real-time polymerase chain reaction (rtPCR-SARS-CoV-2), ultrasensitive C -reactive protein HGNC(usCRP), D-dimer, lactate, dehydrogenase lactate (DHL), erythrocyte sedimentation rate (ESR), ultrasensitive troponin and ferritin.Results:  Compared to placebo group (n=44) with similar baseline characteristics, dutasteride (n=43) presented reduced fatigue, anosmia and overall disease duration (46.6%, 49.6% and 43.2% lower duration, respectively; p<.0001 for all), and in Day 7 presented higher rates of virologic cure (64.3% versus 11.8% cure; p=.0094), , increased recovery rate (84.7% versus 57.5%; p=.03), higher mean [SD] oxygen saturation (97.0% [1.4%] versus 95.7% [2.0%]; p=.02), lower median [IQR] usCRP (0.34mg/L [0.23mg/L -0.66mg/L] versus 1.47mg/L [0.70mg/L-3.37mg/L]; p<.0001),  lower median [IQR] lactate (2.01mmol/L [1.12mmol/L-2.43mmol/L] versus 2.66mmol/L [2.05mmol/L-3.55mmol/L]; p=.0049), lower median [IQR] ESR (5.0mm/1h [3.0mm/1h-11.0mm/1h] versus 14.0mm/1h [7.25mm/1h-18.5mm/1h]; p=.0007), lower median [IQR] LDH (165U/L [144U/L -198U/L] versus 210U/L [179U/L-249U/L]; p=.0013 and lower median [IQR] troponin levels (0.005ng/mL [0.003ng/mL-0.009ng/mL] versus 0.007ng/mL [0.006ng/mL-0.010ng/mL]; p=.048).Conclusions and Relevance: These findings suggest that dutasteride reduces clinical and virologic disease duration and inflammatory markers in males with mild-to-moderate, early-stage COVID-19 MESHD, and should be considered as a therapeutic option in the current context of the COVID-19 pandemic MESHD.Trial Registration: NCT04446429

    Host Cell Proteases Drive Early or Late SARS-CoV-2 Penetration

    Authors: Jana Koch; Zina M Uckeley; Patricio Doldan; Megan L Stanifer; Steeve Boulant; Pierre-Yves Lozach

    doi:10.1101/2020.12.22.423906 Date: 2020-12-23 Source: bioRxiv

    SARS-CoV-2 is a newly emerged coronavirus (CoV) that spread through human populations worldwide in early 2020. CoVs rely on host cell proteases for activation and infection. The trypsin-like protease TMPRSS2 HGNC at the cell surface, cathepsin L HGNC in endolysosomes, and furin HGNC in the Golgi have all been implicated in the SARS-CoV-2 proteolytic processing. Whether SARS-CoV-2 depends on endocytosis internalization and vacuolar acidification for infectious entry remains unclear. Here, we examined the dynamics of SARS-CoV-2 activation during the cell entry process in tissue culture. Using four cell lines representative of lung, colon MESHD, and kidney epithelial tissues, we found that TMPRSS2 HGNC determines the SARS-CoV-2 entry pathways. In TMPRSS2 HGNC-positive cells, infection was sensitive to aprotinin, a TMPRSS2 HGNC inhibitor, but not to SB412515, a drug that impairs cathepsin L HGNC. Infectious penetration was marginally dependent on endosomal acidification, and the virus passed the protease-sensitive step within 10 min. In a marked contrast, in TMPRSS2 HGNC-negative cells cathepsin L HGNC and low pH were required for SARS-CoV-2 entry. The cathepsin L HGNC-activated penetration occurred within 40-60 min after internalization and required intact endolysosomal functions. Importantly, pre-activation of the virus allowed it to bypass the need for endosomal acidification for viral fusion and productive entry. Overall, our results indicate that SARS-CoV-2 shares with other CoVs a strategy of differential use of host cell proteases for activation and infectious penetration. This study also highlights the importance of TMPRSS2 HGNC in dictating the entry pathway used by SARS-CoV-2. SignificancePreventing SARS-CoV-2 spread requires approaches affecting early virus-host cell interactions before the virus enters and infects target cells. Host cell proteases are critical for coronavirus activation and infectious entry. Here, we reconcile apparent contradictory observations from recent reports on endosomal acidification and the role of furin HGNC, TMPRSS2 HGNC, and cathepsin L HGNC in the productive entry and fusion process of SARS-CoV-2. Investigating authentic virus in various cell types, we demonstrated that SARS-CoV-2 developed the ability to use different entry pathways, depending on the proteases expressed by the target cell. Our results have strong implications for future research on the apparent broad tropism of the virus in vivo. This study also provides a handle to develop novel antiviral strategies aiming to block virus entry, as illustrated with the several drugs that we identified to prevent SARS-CoV-2 infection MESHD, some with low IC50.

    Platycodin D prevents both lysosome- and TMPRSS2 HGNC-driven SARS-CoV-2 infection MESHD in vitro by hindering membrane fusion

    Authors: Tai Young Kim; Sangeun Jeon; Youngho Jang; Lizaveta Gotina; Joungha Won; Yeon Ha Ju; Sunpil Kim; Minwoo Wendy Jang; Woojin Won; Mingu Gordon Park; Ae Nim Pae; Sunkyu Han; Seungtaek Kim; C. Justin Lee; Toby Passioura; Richard J Payne

    doi:10.1101/2020.12.22.423909 Date: 2020-12-23 Source: bioRxiv

    An ongoing pandemic of coronavirus disease 2019 MESHD ( COVID-19 MESHD) is now the greatest threat to the global public health. Herbal medicines and their derived natural products have drawn much attention to treat COVID-19 MESHD, but there has been no natural product showing inhibitory activity against SARS-CoV-2 infection MESHD with detailed mechanism. Here, we show that platycodin D (PD), a triterpenoid saponin abundant in Platycodon grandiflorum (PG), a dietary and medicinal herb commonly used in East Asia, effectively blocks the two main SARS-CoV-2 infection MESHD-routes via lysosome- and transmembrane protease, serine 2 ( TMPRSS2 HGNC)-driven entry. Mechanistically, PD prevents host-entry of SARS-CoV-2 by redistributing membrane cholesterol to prevent membrane fusion, which can be reinstated by treatment with a PD-encapsulating agent. Furthermore, the inhibitory effects of PD are recapitulated by a pharmacological inhibition or gene-silencing of NPC1 HGNC, which is mutated in Niemann-Pick type C ( NPC MESHD) patients displaying disrupted membrane cholesterol. Finally, readily available local foods or herbal medicines containing PG root show the similar inhibitory effects against SARS-CoV-2 infection MESHD. Our study proposes that PD is a potent natural product for preventing or treating COVID-19 MESHD and that a brief disruption of membrane cholesterol can be a novel therapeutic approach against SARS-CoV-2 infection MESHD.

    Cardiac SARS-CoV-2 infection MESHD SARS-CoV-2 infection MESHD is associated with distinct transcriptomic changes within the heart

    Authors: Diana Lindner; Hanna Braeuninger; Bastian Stoffers; Antonia Fitzek; Kira Meissner; Ganna Aleshcheva; Michaela Schweizer; Jessica Weimann; Bjoern Rotter; Svenja Warnke; Carolin Edler; Fabian Braun; Kevin Roedl; Katharina Scherschel; Felicitas Escher; Stefan Kluge; Tobias B. Huber; Benjamin Ondruschka; Heinz-Peter Schultheiss; Paulus Kirchhof; Stefan Blankenberg; Klaus Pueschel; Dirk Westermann

    doi:10.1101/2020.12.19.20248542 Date: 2020-12-22 Source: medRxiv

    1BackgroundAnalyses in hospitalized patients and small autopsy series suggest that severe SARS-CoV-2 infection MESHD may affect the heart. We investigated heart tissue by in situ hybridization, immunohistochemistry and RNA sequencing in consecutive autopsy cases to quantify virus load and characterize cardiac involvement in COVID-19 MESHD. MethodsLeft ventricular tissue from 95 deceased with diagnosed SARS-CoV-2 infection MESHD undergoing autopsy was analyzed and clinical data were collected. RNA was isolated to examine virus load of SARS- CoV-2 and its replication in the heart. A virus load >1000 copies per {micro}g RNA was defined as relevant. Viral RNA and inflammatory cells were assessed using histology. RNA sequencing and gene ontology (GO) enrichment were performed in 10 cases with high cardiac virus load and 10 age-matched cases without cardiac infection MESHD. ResultsA relevant SARS-CoV-2 virus load was detected in 41 out of 95 deceased (43%). The median cardiac virus load was 7952 copies per {micro}g RNA (IQR 2507, 32 005). In situ hybridization revealed SARS- CoV-2 RNA primarily in the interstitium or interstitial cells. Virus detection was not associated with increased inflammatory cells. Relevant cardiac infection MESHD was associated with increased expression of the entry factor TMPRSS2 HGNC. Cardiac virus replication was found in 14/95 hearts (15%). Remarkably, cardiac virus replication was associated with shorter time between diagnosis and death MESHD. RNA sequencing revealed clear activation of immune response pathways to virus infection MESHD and destruction of cardiomyocytes. Hearts with high virus load showed activation of the GO term "extracellular exosomes". ConclusionSARS-CoV-2 infection MESHD SARS-CoV-2 infection MESHD including virus replication and distinct transcriptomic alterations without signs of myocarditis MESHD demonstrate a cardiac involvement. In this autopsy series, cardiac replication of SARS-CoV-2 was associated with early death MESHD.

    Furin HGNC cleaves SARS-CoV-2 spike PROTEIN-glycoprotein at S1/S2 and S2'for viral fusion/entry: indirect role for TMPRSS2

    Authors: Rachid Essalmani; Jaspreet Jain; Delia Susan-Resiga; Ursula Andreo; Alexandra Evagelidis; Rabeb Mouna Derbali; David Huynh; Frederic Dallaire; Melanie Laporte; Adrien Delpal; Priscila Sutto-Ortiz; Bruno Coutard; Claudine Mapa; Keith Wilcoxen; Etienne Decroly; Tram Pham; Eric A. Cohen; Nabil G. G Seidah; Massimo Zollo; Achille Iolascon; Mario Capasso; Nour Albes; Hani M. Al-Afghani; Bader Alghamdi; Mansour Almutair; Ebrahim Sabri Mahmoud; Leen Abu Safie; Hadeel El Bardisy; Fawz S. Al Harthi; Abdulraheem Alshareef; Bandar Ali Suliman; Saleh Alqahtani; Abdulaziz AlMalik; May M. Alrashed; Salam Massadeh; Vincent Mooser; Mark Lathrop; Yaseen Arabi; Hamdi Mbarek; Chadi Saad; Wadha Al-Muftah; Radja Badji; Asma Al Thani; Said I. Ismail; Ali G. Gharavi; Malak S. Abedalthagafi; J Brent Richards; David B. Goldstein; Krzysztof Kiryluk

    doi:10.1101/2020.12.18.423106 Date: 2020-12-20 Source: bioRxiv

    The Spike (S)-protein PROTEIN of SARS-CoV-2 binds host-cell receptor ACE2 HGNC and requires proteolytic 'priming' (S1/S2) and 'fusion-activation' (S2') for viral entry. The S-protein PROTEIN furin HGNC-like motifs PRRAR685{downarrow} and KPSKR815{downarrow} indicated that proprotein convertases promote virus entry. We demonstrate that furin HGNC and PC5A induce cleavage at both sites, ACE2 HGNC enhances S2' processing, and their pharmacological inhibition (BOS-inhibitors) block endogenous cleavages. S1/S2-mutations (S1/S2) limit S-protein PROTEIN-mediated cell-to-cell fusion, similarly to BOS-inhibitors. Unexpectedly, TMPRSS2 HGNC does not cleave at S1/S2 or S2', but it can: (i) cleave/inactivate S-protein PROTEIN into S2a/S2b; (ii) shed ACE2 HGNC; (iii) cleave S1-subunit into secreted S1', activities inhibited by Camostat. In lung-derived Calu-3 cells, BOS-inhibitors and S1/S2 severely curtail 'pH-independent' viral entry, and BOS-inhibitors alone/with Camostat potently reduce infectious viral titer and cytopathic effects. Overall, our results show that: furin HGNC plays a critical role in generating fusion-competent S-protein PROTEIN, and indirectly, TMPRSS2 HGNC promotes viral entry, supporting furin HGNC and TMPRSS2 HGNC inhibitors as potential antivirals against SARS-CoV-2

    Common variants at 21q22.3 locus influence MX1 HGNC gene expression and susceptibility to severe COVID-19 MESHD

    Authors: Immacolata Andolfo; Roberta Russo; Alessandro Vito Lasorsa; Sueva Cantalupo; Barbara Eleni Rosato; Ferdinando Bonfiglio; Giulia Frisso; Pasquale Abete; Gian Marco Cassese; Giuseppe Servillo; Gabriella Esposito; Ivan Gentile; Carmelo Piscopo; Romolo Villani; Giuseppe Fiorentino; Pellegrino Cerino; Carlo Buonerba; Biancamaria Pierri; Massimo Zollo; Achille Iolascon; Mario Capasso

    doi:10.1101/2020.12.18.20248470 Date: 2020-12-20 Source: medRxiv

    The COVID-19 MESHD disease, caused by the SARS-Cov-2, presents a heterogeneous clinical spectrum. The risk factors do not fully explain the wide spectrum of disease manifestations, so it is possible that genetic factors could account for novel insights into its pathogenesis. In our previous study, we hypothesized that common variants on chromosome 21, near TMPRSS2 HGNC and MX1 HGNC genes, may be genetic risk factors associated to the different clinical manifestations of COVID-19 MESHD. Here, we performed an in-depth genetic analysis of chromosome 21 exploiting the genome-wide association study data including 6,406 individuals hospitalized for COVID-19 MESHD and 902,088 controls with European genetic ancestry from COVID-19 MESHD Host Genetics Initiative. We found that five single nucleotide polymorphisms (SNPs) within TMPRSS2 HGNC and near MX1 HGNC gene show suggestive associations (P[≤]1x10-5) with severe COVID-19 MESHD. All five SNPs replicated the association in two independent cohorts of Asian subjects while two and one out of the 5 SNPs replicated in African and Italian populations, respectively (P[≤]0.05). The minor alleles of these five SNPs correlated with a reduced risk of developing severe COVID-19 MESHD and increased level of MX1 HGNC expression in blood. Our findings provide further evidence that host genetic factors can contribute to determine the different clinical presentations of COVID-19 MESHD and that MX1 HGNC, an antiviral effector of type I and III interferon pathway, may be a potential therapeutic target.

    Profiling of oral microbiota and cytokines in COVID-19 MESHD patients

    Authors: Valerio Iebba; Nunzia Zanotta; Giuseppina Campisciano; Verena Zerbato; Stefano Di Bella; Carolina Cason; Sara Morassut; Roberto Luzzati; Marco Confalonieri; Anna Teresa Palamara; Manola Comar

    doi:10.1101/2020.12.13.422589 Date: 2020-12-14 Source: bioRxiv

    SARS-CoV-2 presence has been recently demonstrated in the sputum or saliva, suggesting how the shedding of viral RNA outlasts the end of symptoms. Recent data from transcriptome analysis show that oral cavity mucosa harbors high levels of ACE2 HGNC and TMPRSS2 HGNC, highlighting its role as a double-edged sword for SARS-CoV-2 body entrance or interpersonal transmission. In the present study, for the first time, we demonstrate the oral microbiota structure and inflammatory profile of COVID-19 MESHD patients. Hospitalized COVID-19 MESHD patients and matched healthy controls underwent naso/oral-pharyngeal and oral swabs. Microbiota structure was analyzed by 16S rRNA V2 automated targeted sequencing, while oral and sera concentrations of 27 cytokines were assessed using magnetic bead-based multiplex immunoassays. A significant diminution in species richness was observed in COVID-19 MESHD patients, along with a marked difference in beta-diversity. Species such as Prevotella salivae and Veillonella infantium were distinctive for COVID-19 MESHD patients, while Neisseria perflava and Granulicatella elegans were predominant in controls. Interestingly, these two groups of oral species oppositely clustered within the bacterial network, defining two distinct Species Interacting Group (SIGs). Pro-inflammatory cytokines were distinctive for COVID-19 MESHD in both oral and serum samples, and we found a specific bacterial consortium able to counteract them, following a novel index called C4 firstly proposed here. We even introduced a new parameter, named CytoCOV, able to predict COVID-19 MESHD susceptibility for an unknown subject at 71% of power with an AUC equal to 0.995. This pilot study evidenced a distinctive oral microbiota composition in COVID-19 MESHD subjects, with a definite structural network in relation to secreted cytokines. Our results would pave the way for a theranostic approach in fighting COVID-19 MESHD, trying to enlighten the intimate relationship among microbiota and SARS-CoV-2 infection MESHD.

    Evaluation of SARS-CoV-2 neutralization assays for antibody monitoring in natural infection and vaccine trials

    Authors: Anton M Sholukh; Andrew Fiore-Gartland; Emily S Ford; Yixuan Hou; Longping Victor Tse; Florian A Lempp; Hanna Kaiser; Russell Saint Germain; Emily Bossard; Jia Jin Kee; Kurt Diem; Andrew B Stuart; Peter B Rupert; Chance Brock; Matthew Buerger; Margaret K Doll; April Kaur Randhawa; Leonidas Stamatatos; Roland K Strong; Colleen McLaughlin; Keith R. Jerome; Ralph S. Baric; David Montefiori; Lawrence Corey

    doi:10.1101/2020.12.07.20245431 Date: 2020-12-08 Source: medRxiv

    Determinants of protective immunity against SARS-CoV-2 infection MESHD require the development of well-standardized, reproducible antibody assays to be utilized in concert with clinical trials to establish correlates of risk and protection. This need has led to the appearance of a variety of neutralization assays used by different laboratories and companies. Using plasma samples from COVID-19 MESHD convalescent individuals with mild-to-moderate disease from a localized outbreak in a single region of the western US, we compared three platforms for SARS-CoV-2 neutralization: assay with live SARS-CoV-2, pseudovirus assay utilizing lentiviral (LV) and vesicular stomatitis virus MESHD ( VSV MESHD) packaging, and a surrogate ELISA test. Vero, Vero E6, HEK293T cells expressing human angiotensin converting enzyme 2 HGNC ( hACE2 HGNC), and TZM-bl cells expressing hACE2 HGNC and transmembrane serine protease 2 ( TMPRSS2 HGNC) were evaluated. Live-virus and LV-pseudovirus assay with HEK293T cells showed similar geometric mean titers (GMTs) ranging 141-178, but VSV MESHD-pseudovirus assay yielded significantly higher GMT (310 95%CI 211-454; p < 0.001). Fifty percent neutralizing dilution (ND50) titers from live-virus and all pseudovirus assay readouts were highly correlated (Pearson r = 0.81-0.89). ND50 titers positively correlated with plasma concentration of IgG against SARS-CoV-2 spike PROTEIN and receptor binding domain (RBD) (r = 0.63-0.89), but moderately correlated with nucleoprotein PROTEIN IgG (r = 0.46-0.73). There was a moderate positive correlation between age and spike (Spearmans rho=0.37, p=0.02), RBD (rho=0.39, p=0.013) and nucleoprotein PROTEIN IgG (rho=0.45, p=0.003). ND80 showed stronger correlation with age than ND50 (ND80 rho=0.51 (p=0.001), ND50 rho=0.28 (p=0.075)). Our data demonstrate high concordance between cell-based assays with live and pseudotyped virions.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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