Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (576)

NSP5 (29)

ProteinN (23)

ComplexRdRp (22)

ProteinS1 (21)


SARS-CoV-2 Proteins
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    Interferon-regulated genetic programs and JAK/STAT pathway activate the intronic promoter of the short ACE2 HGNC isoform in renal proximal tubules

    Authors: Yue Wan; Siwy Ling Yang; Louis DeFalco; Danielle E Anderson; Yu Zhang; Ashley J Aw; Su Ying Lim; Xin Ni Lim; Kiat Yee Tan; Tong Zhang; Tanu Chawla; Yan Su; Alexander Lezhava; Paola de Sessions; Andres Merits; Lin-Fa Wang; Roland G Huber; Catherine M. Green; Teresa Lambe; Peijun Zhang; Sarah C Gilbert; Max Crispin; Roshni Patel; Juan P Dizon; Irina Shimeliovich; Anna Gazumyan; Marina Caskey; Pamela J Bjorkman; Rafael Casellas; Theodora Hatziioannou; Paul D Bieniasz; Michel C Nussenzweig

    doi:10.1101/2021.01.15.426908 Date: 2021-01-19 Source: bioRxiv

    Summary: Recently, a short, interferon-inducible isoform of Angiotensin-Converting Enzyme 2 ( ACE2 HGNC), dACE2 was identified. ACE2 HGNC is a SARS-Cov-2 receptor and changes in its renal expression have been linked to several human nephropathies MESHD. These changes were never analyzed in context of dACE2, as its expression was not investigated in the kidney. We used Human Primary Proximal Tubule (HPPT) cells to show genome-wide gene expression patterns after cytokine stimulation, with emphasis on the ACE2 HGNC/dACE2 locus. Putative regulatory elements controlling dACE2 expression were identified using ChIP-seq and RNA-seq. qRT-PCR differentiating between ACE2 HGNC and dACE2 revealed 300- and 600-fold upregulation of dACE2 by IFN and IFN{beta}, respectively, while full length ACE2 HGNC expression was almost unchanged. JAK inhibitor ruxolitinib ablated STAT1 HGNC and dACE2 expression after interferon treatment. Finally, with RNA-seq, we identified a set of genes, largely immune-related, induced by cytokine treatment. These gene expression profiles provide new insights into cytokine response of proximal tubule cells.

    BRD2 HGNC inhibition blocks SARS-CoV-2 infection MESHD in vitro by reducing transcription of the host cell receptor ACE2

    Authors: Ruilin Tian; Avi J Samelson; Veronica V Rezelj; Merissa Chen; Gokul N Ramadoss; Xiaoyan Guo; Alice Mac Kain; Quang Dinh Tran; Shion A Lim; Irene Lui; James Nunez; Sarah J Rockwood; Na Liu; Jared Carlson-Stevermer; Jennifer Oki; Travis Maures; Kevin Holden; Jonathan S Weissman; James A Wells; Bruce Conklin; Marco Vignuzzi; Martin Kampmann; Roshni Patel; Juan P Dizon; Irina Shimeliovich; Anna Gazumyan; Marina Caskey; Pamela J Bjorkman; Rafael Casellas; Theodora Hatziioannou; Paul D Bieniasz; Michel C Nussenzweig

    doi:10.1101/2021.01.19.427194 Date: 2021-01-19 Source: bioRxiv

    SARS-CoV-2 infection MESHD of human cells is initiated by the binding of the viral Spike protein PROTEIN to its cell-surface receptor ACE2 HGNC. We conducted an unbiased CRISPRi screen to uncover druggable pathways controlling Spike protein PROTEIN binding to human cells. We found that the protein BRD2 HGNC is an essential node in the cellular response to SARS-CoV-2 infection MESHD. BRD2 HGNC is required for ACE2 HGNC transcription in human lung epithelial cells and cardiomyocytes, and BRD2 HGNC inhibitors currently evaluated in clinical trials potently block endogenous ACE2 HGNC expression and SARS-CoV-2 infection MESHD of human cells. BRD2 HGNC also controls transcription of several other genes induced upon SARS-CoV-2 infection MESHD, including the interferon response, which in turn regulates ACE2 HGNC levels. It is possible that the previously reported interaction between the viral E protein PROTEIN and BRD2 HGNC evolved to manipulate the transcriptional host response during SARS-CoV-2 infection MESHD. Together, our results pinpoint BRD2 HGNC as a potent and essential regulator of the host response to SARS-CoV-2 infection MESHD and highlight the potential of BRD2 HGNC as a novel therapeutic target for COVID-19 MESHD.

    Azithromycin Plus Zinc Sulfate Rapidly and Synergistically Suppresses IκBα HGNC-Mediated In Vitro Human Airway Cell ACE2 HGNC Expression for SARS-CoV-2 Entry

    Authors: Yin-Kai Chen; Tsung-Tao Huang; Chia-Wei Chang; Ming-Cheng Lee; Bor-Ru Lin; Yen-Pei Lu; Yih-Jen Hsu; Chun-Yu Chuang; Nathen E Bopp; Patricia V Aguilar; Ping Ren; Vineet D Menachery; Michael S Diamond; Scott C Weaver; Xuping Xie; Pei-Yong Shi; Udeni BR Balasuriya; Adolfo Garcia-Sastre; Juergen A Richt; Marit J van Gils; Laura E McCoy; Max Crispin; Roshni Patel; Juan P Dizon; Irina Shimeliovich; Anna Gazumyan; Marina Caskey; Pamela J Bjorkman; Rafael Casellas; Theodora Hatziioannou; Paul D Bieniasz; Michel C Nussenzweig

    doi:10.1101/2021.01.19.427206 Date: 2021-01-19 Source: bioRxiv

    Large-scale efforts have been persistently undertaken for medical prophylaxis and treatment of COVID-19 MESHD disasters worldwide. A variety of novel viral spike protein PROTEIN-targeted vaccine preparations have recently been clinically distributed based on accelerated approval. We revisited the early but inconclusive clinical interest in the combination of azithromycin and zinc sulfate repurposing with safety advantages. In vitro proof of concept was provided for rapid and synergistic suppression of ACE2 HGNC expression following treatments in human airway cells, Calu-3 and H322M. The two representative ACE2 HGNC-expressing human airway cells indicate the upper and lower respiratory tracts. Prophylactic and early therapeutic roles of azithromycin combined with zinc are proposed for virus cellular entry prevention potential bridging to effective antibody production.

    A trans-complementation system for SARS-CoV-2

    Authors: Xianwen Zhang; Yang Liu; Jianying Liu; Adam L Bailey; Kenneth S Plante; Jessica A Plante; Jing Zou; Hongjie Xia; Nathen E Bopp; Patricia V Aguilar; Ping Ren; Vineet D Menachery; Michael S Diamond; Scott C Weaver; Xuping Xie; Pei-Yong Shi; Udeni BR Balasuriya; Adolfo Garcia-Sastre; Juergen A Richt; Marit J van Gils; Laura E McCoy; Max Crispin; Roshni Patel; Juan P Dizon; Irina Shimeliovich; Anna Gazumyan; Marina Caskey; Pamela J Bjorkman; Rafael Casellas; Theodora Hatziioannou; Paul D Bieniasz; Michel C Nussenzweig

    doi:10.1101/2021.01.16.426970 Date: 2021-01-19 Source: bioRxiv

    The biosafety level-3 (BSL-3) requirement to culture severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2) is a bottleneck for research and countermeasure development. Here we report a trans-complementation system that produces single-round infectious SARS-CoV-2 that recapitulates authentic viral replication. We demonstrate that the single-round infectious SARS-CoV-2 can be used at BSL-2 laboratories for high-throughput neutralization and antiviral testing. The trans-complementation system consists of two components: a genomic viral RNA containing a deletion of ORF3 HGNC and envelope gene, and a producer cell line expressing the two deleted genes. Trans-complementation of the two components generates virions that can infect naive cells for only one round, but does not produce wild-type SARS-CoV-2. Hamsters and K18- hACE2 HGNC transgenic mice inoculated with the complementation-derived virions exhibited no detectable disease, even after intracranial inoculation with the highest possible dose. The results suggest that the trans-complementation platform can be safely used at BSL-2 laboratories for research and countermeasure development.

    Tropism of SARS-CoV-2 MESHD for Developing Human Cortical Astrocytes

    Authors: Madeline G Andrews; Tanzila Mukhtar; Ugomma C Eze; Camille R Simoneau; Yonatan Perez; Mohammed A Mostajo-Radji; Shaohui Wang; Dmitry Velmeshev; Jahan Salma; G. Renuka Kumar; Alex A Pollen; Elizabeth E Crouch; Melanie Ott; Arnold R Kriegstein

    doi:10.1101/2021.01.17.427024 Date: 2021-01-18 Source: bioRxiv

    The severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2) readily infects MESHD a variety of cell types impacting the function of vital organ systems, with particularly severe impact on respiratory function. It proves fatal for one percent of those infected. Neurological symptoms MESHD, which range in severity, accompany a significant proportion of COVID-19 MESHD cases, indicating a potential vulnerability of neural cell types. To assess whether human cortical cells can be directly infected by SARS-CoV-2, we utilized primary human cortical tissue and stem cell-derived cortical organoids. We find significant and predominant infection in cortical astrocytes in both primary and organoid cultures, with minimal infection of other cortical populations. Infected astrocytes had a corresponding increase in reactivity characteristics, growth factor signaling, and cellular stress. Although human cortical cells, including astrocytes, have minimal ACE2 HGNC expression, we find high levels of alternative coronavirus receptors in infected astrocytes, including DPP4 HGNC and CD147 HGNC. Inhibition of DPP4 HGNC reduced infection and decreased expression of the cell stress marker, ARCN1 HGNC. We find tropism of SARS-CoV-2 MESHD for human astrocytes mediated by DPP4 HGNC, resulting in reactive gliosis-type injury MESHD.

    Insights from a Pan India Sero-Epidemiological survey (Phenome-India Cohort) for SARS-CoV2

    Authors: Salwa Naushin; Viren Sardana; Rajat Ujjainiya; Nitin Bhatheja; Rintu Kutum; Akash Kumar Bhaskar; Shalini Pradhan; Satyartha Prakash; Raju Khan; Birendra Singh Rawat; Giriraj Ratan Chandak; Karthik Bharadwaj Tallapaka; Mahesh Anumalla; Amit Lahiri; Susanta Kar; Shrikant Ramesh Mulay; Madhav Nilakanth Mugale; Mrigank Srivastava; Shaziya Khan; Anjali Srivastava; Bhawna Tomar; Murugan Veerapandian; Ganesh Venkatachalam; Selvamani Raja Vijayakumar; Ajay Agarwal; Dinesh Gupta; Prakash M Halami; Muthukumar Serva Peddha; Gopinath M; Ravindra P Veeranna; Anirban Pal; Vinay Kumar Agarwal; Anil Ku Maurya; Ranvijay Kumar Singh; Ashok Kumar Raman; Suresh Kumar Anandasadagopan; Parimala Karupannan; Subramanian Venkatesan; Harish Kumar Sardana; Anamika Kothari; Rishabh Jain; Anupma Thakur; Devendra Singh Parihar; Anas Saifi; Jasleen Kaur; Virendra Kumar; Avinash Mishra; Iranna Gogeri; Geetha Vani Rayasam; Praveen Singh; Rahul Chakraborty; Gaura Chaturvedi; Pinreddy Karunakar; Rohit Yadav; Sunanda Singhmar; Dayanidhi Singh; Sharmistha Sarkar; Purbasha Bhattacharya; Sundaram Acharya; Vandana Singh; Shweta Verma; Drishti Soni; Surabhi Seth; Firdaus Fatima; Shakshi Vashisht; Sarita Thakran; Akash Pratap Singh; Akanksha Sharma; Babita Sharma; Manikandan Subramanian; Yogendra Padwad; Vipin Hallan; Vikram Patial; Damanpreet Singh; Narendra Vijay Tirpude; Partha Chakrabarti; Sujay Krishna Maity; Dipyaman Ganguly; Jit Sarkar; Sistla Ramakrishna; Balthu Narender Kumar; Kiran A Kumar; Sumit G. Gandhi; Piyush Singh Jamwal; Rekha Chouhan; Vijay Lakshmi Jamwal; Nitika Kapoor; Debashish Ghosh; Ghanshyam Thakkar; Umakanta Subudhi; Pradip Sen; Saumya Raychaudhri; Amit Tuli; Pawan Gupta; Rashmi Kumar; Deepak Sharma; Rajesh P. Ringe; Amarnarayan D; Mahesh Kulkarni; Dhanasekaran Shanmugam; Mahesh Dharne; Syed G Dastager; Rakesh Joshi; Amita P. Patil; Sachin N Mahajan; Abu Junaid Khan; Vasudev Wagh; Rakeshkumar Yadav; Ajinkya Khilari; Mayuri Bhadange; Arvindkumar H. Chaurasiya; Shabda E Kulsange; Krishna khairnar; Shilpa Paranjape; Jatin Kalita; G.Narahari Sastry; Tridip Phukan; Prasenjit Manna; Wahengbam Romi; Pankaj Bharali; Dibyajyoti Ozah; Ravi Kumar Sahu; Elapaval VSSK Babu; Rajeev K Sukumaran; Aishwarya R Nair; Anoop Puthiyamadam; Prajeesh Kooloth Valappil; Adarsh Velayudhanpillai; Kalpana Chodankar; Samir Damare; Yennapu Madhavi; Ved Varun Agrawal; Sumit Dahiya; Anurag Agrawal; Debasis Dash; Shantanu Sengupta

    doi:10.1101/2021.01.12.21249713 Date: 2021-01-16 Source: medRxiv

    BackgroundIndia has been amongst the most affected nations during the SARS-CoV2 pandemic, with sparse data on country-wide spread of asymptomatic infections and antibody persistence. This longitudinal cohort study was aimed to evaluate SARS-CoV2 sero-positivity rate as a marker of infection and evaluate temporal persistence of antibodies with neutralization capability and to infer possible risk factors for infection. MethodsCouncil of Scientific and Industrial Research, India (CSIR) with its more than 40 laboratories and centers in urban and semi-urban settings spread across the country piloted the pan country surveillance. 10427 adult individuals working in CSIR laboratories and their family members based on voluntary participation were assessed for antibody presence and stability was analyzed over 6 months utilizing qualitative Elecsys SARS CoV2 specific antibody kit and GENScript cPass SARS-CoV2 Neutralization Antibody Detection Kit. Along with demographic information, possible risk factors were evaluated through self to be filled online forms with data acquired on blood group type, occupation type, addiction and habits including smoking and alcohol, diet preferences, medical history and transport type utilized. Symptom history and information on possible contact and compliance with COVID 19 universal precautions was also obtained. Findings1058 individuals (10{middle dot}14%) had antibodies against SARS-CoV2. A follow-up on 346 sero-positive individuals after three months revealed stable to higher antibody levels against SARS-CoV2 but declining plasma activity for neutralizing SARS-CoV2 receptor binding domain and ACE2 HGNC interaction. A repeat sampling of 35 individuals, at six months, revealed declining antibody levels while the neutralizing activity remained stable compared to three months. Majority of sero-positive individuals (75%) did not recall even one of nine symptoms since March 2020. Fever MESHD was the most common symptom with one-fourth reporting loss of taste or smell. Significantly associated risks for sero-positivity (Odds Ratio, 95% CI, p value) were observed with usage of public transport (1{middle dot}79, 1{middle dot}43 - 2{middle dot}24, 2{middle dot}81561E-06), occupational responsibilities such as security, housekeeping personnel etc. (2{middle dot}23, 1{middle dot}92 - 2{middle dot}59, 6{middle dot}43969E-26), non-smokers (1{middle dot}52, 1{middle dot}16 - 1{middle dot}99, 0{middle dot}02) and non-vegetarianism MESHD (1{middle dot}67, 1{middle dot}41 - 1{middle dot}99, 3{middle dot}03821E-08). An iterative regression analysis was confirmatory and led to only modest changes to estimates. Predilections for sero-positivity was noted with specific ABO blood groups -O was associated with a lower risk. InterpretationIn a first-of-its-kind study from India, we report the sero-positivity in a country-wide cohort and identify variable susceptible associations for contacting infection. Serology and Neutralizing Antibody response provides much-sought-for general insights on the immune response to the virus among Indians and will be an important resource for designing vaccination strategies. FundingCouncil of Scientific and Industrial Research, India (CSIR)

    Host-cell recognition through GRP78 HGNC is enhanced in the new UK variant of SARS-CoV-2, in silico 

    Authors: Abdo A Elfiky; Ibrahim M Ibrahim

    doi:10.21203/ Date: 2021-01-15 Source: ResearchSquare

    New SARS-CoV-2 variant VUI 202012/01 started in the UK and currently spreading in Europe and Australia during the last few days. The new variant bears about nine mutations in the spike protein PROTEIN (Δ69-70, Δ145, N501Y, A570D, D614G, P681H, T716I, S982A, and D1118H). The N501Y lies in the receptor-binding domain (RBD) of the spike and interacts with the host-cell receptor A CE2 HGNCresponsible for viral recognition and entry. We tried to simulate the system of A CE2- HGNC SARS-CoV-2 spike PROTEIN RBD in the wildtype and mutated isoform of the RBD (N501Y). Additionally, the G RP78 HGNCassociation with the A CE2- HGNC SARS-CoV-2 spike PROTEIN RBD is modeled at the presence of this mutant variant of the viral spike. 

    The lethal triad: SARS-CoV-2 Spike MESHD SARS-CoV-2 Spike PROTEIN, ACE2 HGNC and TMPRSS2 HGNC. Mutations in host and pathogen may affect the course of pandemic.

    Authors: Matteo Calcagnile; Patricia Forgez; Pietro Alifano; Marco Alifano; Leonardo C Caserta; Patrick K. Mitchell; Eric Cassmann; Alicia Rollins; Nancy C Zylich; Randall Wayne Renshaw; Cassandra Guarino; Bettina Wagner; Kelly Lager; Diego G Diel; Sankar Bhattacharyya; Samreen Siddiqui; Akansha Tyagi; Sujeet Jha; Rajesh Pandey; Somnath Dutta; Rajesh P. Ringe; Raghavan Varadarajan; Louis-Marie Bloyet; Fabio Benigni; Elisabetta Cameroni; Johan Neyts; Agostino Riva; Gyorgy Snell; Amalio Telenti; Sean PJ Whelan; Herbert W Virgin; Davide Corti; Matteo Samuele Pizzuto; David Veesler

    doi:10.1101/2021.01.12.426365 Date: 2021-01-14 Source: bioRxiv

    Variants of SARS-CoV-2 have been identified rapidly after the beginning of pandemic. One of them, involving the spike protein PROTEIN and called D614G, represents a substantial percentage of currently isolated strains. While research on this variant was ongoing worldwide, on December 20th 2020 the European Centre for Disease Prevention and Control reported a Threat Assessment Brief describing the emergence of a new variant of SARS-CoV-2, named B.1.1.7, harboring multiple mutations mostly affecting the Spike protein PROTEIN. This viral variant has been recently associated with a rapid increase in COVID-19 MESHD cases in South East England, with alarming implications for future virus transmission rates. Specifically, of the nine amino acid replacements that characterize the Spike in the emerging variant, four are found in the region between the Fusion Peptide and the RBD domain (namely the already known D614G, together with A570D, P681H, T716I), and one, N501Y, is found in the Spike Receptor Binding Domain - Receptor Binding Motif (RBD- RBM HGNC). In this study, by using in silico biology, we provide evidence that these amino acid replacements have dramatic effects on the interactions between SARS-CoV-2 Spike PROTEIN SARS-CoV-2 Spike MESHD and the host ACE2 receptor or TMPRSS2 HGNC, the protease that induces the fusogenic activity of Spike. Mostly, we show that these effects are strongly dependent on ACE2 HGNC and TMPRSS2 HGNC polymorphism, suggesting that dynamics of pandemics are strongly influenced not only by virus variation but also by host genetic background.

    Fatal neuroinvasion of SARS-CoV-2 in K18- hACE2 HGNC mice is partially dependent on hACE2 HGNC expression

    Authors: Mariano Carossino; Paige Montanaro; Devin Kenney; Hans Gertje; Kyle Grosz; Susanna Kurnick; Markus Bosmann; Mohsan Saeed; Udeni Balasuriya; Florian Douam; Nicholas Crossland; Madison M Hebert; Scott W Benzinger; Koushik T Sinha; Keith T Gagnon; Rafael Rezende; Eduardo Cilli; Guilherme Malafaia; Nicholas Thomson; Caroline Buckee; Firdausi Qadri; Tahmina Shirin

    doi:10.1101/2021.01.13.425144 Date: 2021-01-13 Source: bioRxiv

    Animal models recapitulating the distinctive features of severe COVID-19 MESHD are critical to enhance our understanding of SARS-CoV-2 pathogenesis. Transgenic mice expressing human angiotensin-converting enzyme 2 HGNC ( hACE2 HGNC) under the cytokeratin 18 promoter ( K18 HGNC- hACE2 HGNC) represent a lethal model of SARS-CoV-2 infection MESHD. However, the cause(s) and mechanisms of lethality in this mouse model remain unclear. Here, we evaluated the spatiotemporal dynamics of SARS-CoV-2 infection MESHD for up to 14 days post-infection. Despite infection and moderate inflammation MESHD in the lungs, lethality was invariably associated with viral neuroinvasion and neuronal damage MESHD (including spinal motor neurons). Neuroinvasion occurred following virus transport through the olfactory neuroepithelium in a manner that was only partially dependent on hACE2 HGNC. Interestingly, SARS-CoV-2 tropism MESHD was overall neither widespread among nor restricted to only ACE2-expressing cells. Although our work incites caution in the utility of the K18- hACE2 HGNC model to study global aspects of SARS-CoV-2 pathogenesis, it underscores this model as a unique platform for exploring the mechanisms of SARS-CoV-2 neuropathogenesis MESHD. SUMMARY COVID-19 MESHD is a respiratory disease MESHD caused by SARS-CoV-2, a betacoronavirus. Here, we show that in a widely used transgenic mouse model of COVID-19 MESHD, lethality is invariably associated with viral neuroinvasion and the ensuing neuronal disease MESHD, while lung inflammation MESHD remains moderate.

    Molecular dynamic simulation reveals E484K mutation enhances spike RBD- ACE2 HGNC affinity and the combination of E484K, K417N and N501Y mutations (501Y.V2 variant) induces conformational change greater than N501Y mutant alone, potentially resulting in an escape mutant

    Authors: Gard Nelson; Oleksandr Buzko; Patricia R Spilman; Kayvan Niazi; Shahrooz Rabizadeh; Patrick R Soon-Shiong; Ola Spjuth; Marjo-Riitta Puumalainen; Jordi Carreras-Puigvert; Rafael H Nobrega; Giovane Galdino; Antonio Condino-Neto; Jorge Galindo-Villegas; Glaucia Machodo-Santelli; Paulo Sanches; Rafael Rezende; Eduardo Cilli; Guilherme Malafaia; Nicholas Thomson; Caroline Buckee; Firdausi Qadri; Tahmina Shirin

    doi:10.1101/2021.01.13.426558 Date: 2021-01-13 Source: bioRxiv

    Rapidly spreading SARS-CoV-2 variants present not only an increased threat to human health due to the confirmed greater transmissibility of several of these new strains but, due to conformational changes induced by the mutations, may render first-wave SARS-CoV-2 convalescent sera, vaccine-induced antibodies, or recombinant neutralizing antibodies (nAbs) ineffective. To be able to assess the risk of viral escape from neutralization by first-wave antibodies, we leveraged our capability for Molecular Dynamic ( MD MESHD) simulation of the spike receptor binding domain (S RBD) and its binding to human angiotensin-converting enzyme 2 HGNC ( hACE2 HGNC) to predict alterations in molecular interactions resulting from the presence of the E484K, K417N, and N501Y variants found in the South African 501Y.V2 strain - alone and in combination. We report here the combination of E484K, K417N and N501Y results in the highest degree of conformational alterations of S RBD when bound to hACE2 HGNC, compared to either E484K or N501Y alone. Both E484K and N501Y increase affinity of S RBD for hACE2 HGNC and E484K in particular switches the charge on the flexible loop region of RBD which leads to the formation of novel favorable contacts. Enhanced affinity of S RBD for hACE2 HGNC very likely underpins the greater transmissibility conferred by the presence of either E484K or N501Y; while the induction of conformational changes may provide an explanation for evidence that the 501Y.V2 variant, distinguished from the B.1.1.7 UK variant by the presence of E484K, is able to escape neutralization by existing first-wave anti-SARS-CoV-2 antibodies and re-infect COVID-19 MESHD convalescent individuals.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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