Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (24)

NSP5 (1)

ProteinN (1)

ComplexRdRp (1)


SARS-CoV-2 Proteins
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    Qualitatively distinct modes of Sputnik V vaccine-neutralization escape by SARS-CoV-2 Spike PROTEIN variants

    Authors: Satoshi Ikegame; Mohammed N. A. Siddiquey; Chuan-Tien Hung; Griffin Haas; Luca Brambilla; Kasopefoluwa Y. Oguntuyo; Shreyas Kowdle; Ariel Esteban Vilardo; Alexis Edelstein; Claudia Perandones; Jeremy P. Kamil; Benhur Lee

    doi:10.1101/2021.03.31.21254660 Date: 2021-04-02 Source: medRxiv

    The novel pandemic betacoronavirus, severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), has infected at least 120 million people since its identification as the cause of a December 2019 viral pneumonia MESHD outbreak in Wuhan, China. Despite the unprecedented pace of vaccine development, with six vaccines already in use worldwide, the emergence of SARS-CoV-2 variants of concern (VOC) across diverse geographic locales suggests herd immunity may fail to eliminate the virus. All three officially designated VOC carry Spike (S) polymorphisms thought to enable escape from neutralizing antibodies elicited during initial waves of the pandemic. Here, we characterize the biological consequences of the ensemble of S mutations present in VOC lineages B.1.1.7 (501Y.V1) and B.1.351 (501Y.V2). Using a replication-competent EGFP-reporter vesicular stomatitis virus MESHD ( VSV MESHD) system, rcVSV-CoV2-S, which encodes S from SARS coronavirus 2 in place of VSV MESHD-G, coupled with a clonal HEK-293T ACE2 HGNC TMPRSS2 cell line optimized for highly efficient S-mediated infection, we determined that 8 out of 12 (75%) of serum samples from 12 recipients of the Russian Sputnik V Ad26 / Ad5 vaccine showed dose response curve slopes indicative of failure to neutralize rcVSV-CoV2-S: B.1.351. The same set of sera efficiently neutralized S from B.1.1.7 and showed only moderately reduced activity against S carrying the E484K substitution alone. Taken together, our data suggest that control of emergent SARS-CoV-2 variants may benefit from updated vaccines.

    A time series forecasting of the proportion of SARS-CoV-2 N501Y lineage in North America

    Authors: Elena Quinonez; Majid Vahed; Abdolrazagh Hashemi Shahraki; Mehdi Mirsaeidi

    doi:10.1101/2021.03.30.21254648 Date: 2021-03-31 Source: medRxiv

    Introduction: The outbreak of pneumonia MESHD known as SARS-COV-2 and newly-emerging South African (B.1.351), the United Kingdom (B.1.1.7) and Brazil (P.1) variants have led to a more infectious virus and potentially more substantial loss of neutralizing activity by natural infection or vaccine-elicited antibodies. Methods: We identified prevalent mutations using the spike receptor-binding domain (S-RBD) of SARS-CoV-2 deposited in the Nextstrain global database and comparing them to the Wuhan-Hu-1/2019 genomic sequence as a reference. Then we calculated the percentages of mutant genomes from the total regional subsample isolates from December 2019 to the end of January 2021. We developed two separate time series forecasting models for the SARS-CoV-2 B.1.1.7 variant. The computational model used the structure of the S-RBD to examine its interactions with the neutralizing antibody, named CV30 (isolated from a patient), and human angiotensin-converting enzyme 2 HGNC ( hACE-2 HGNC), based on a hybrid algorithm of template-based modeling to predict the affinity of S protein PROTEIN to the neutralizing antibodies and hACE-2 receptor. Results: The proportion of the B.1.1.7 strain in North America is growing fast. From these computations, it seems that the S-RBD and hACE-2 HGNC proteins are less favorable for the South African strain (K417N, E484K, and N501Y) as compared to the wild type structure and more favorable for B.1.1.7 and P.1 variants. In the present of crystallized CV30 neutralizing antibodies, docking scores suggest antibodies can be partially neutralize the B.1.1.7 variant, and, less efficiently, the B.1.351 and P.1 variants. Conclusion: The rapid evolution of SARS-CoV-2 has the potential to allow the newly-emerged B.1.351, and P.1 variants to escape from natural or vaccine-induced neutralizing immunity and viral spreading.

    Circadian regulation of SARS-CoV-2 infection MESHD in lung epithelial cells

    Authors: Xiaodong Zhuang; Senko Tsukuda; Florian Wrensch; Peter AC Wing; Helene Borrmann; James M Harris; Sophie B Morgan; Laurent Mailly; Nazia Thakur; Carina Conceicao; Harshmeena Sanghani; Laura Heydmann; Charlotte Bach; Anna Ashton; Steven Walsh; Tiong Kit Tan; Lisa Schimanski; Kuan-Ying A Huang; Catherine Schuster; Koichi Watashi; Timothy SC Hinks; Aarti Jagannath; Sridhar R Vausdevan; Dalan Bailey; Thomas F Baumert; Jane A McKeating

    doi:10.1101/2021.03.20.436163 Date: 2021-03-21 Source: bioRxiv

    The COVID-19 pandemic MESHD, caused by SARS-CoV-2 coronavirus MESHD, is a global health issue with unprecedented challenges for public health. SARS-CoV-2 primarily infects cells of the respiratory tract, via binding human angiotensin-converting enzyme ( ACE2 HGNC), and infection can result in pneumonia MESHD and acute respiratory distress syndrome MESHD. Circadian rhythms coordinate an organisms response to its environment and recent studies report a role for the circadian clock to regulate host susceptibility to virus infection MESHD. Influenza A infection of arhythmic mice, lacking the circadian component BMAL1, results in higher viral replication and elevated inflammatory responses leading to more severe bronchitis MESHD, highlighting the impact of circadian pathways in respiratory function. We demonstrate circadian regulation of ACE2 in lung epithelial cells and show that silencing BMAL1 or treatment with the synthetic REV-ERB agonist SR9009 reduces ACE2 expression and inhibits SARS-CoV-2 entry MESHD and RNA replication. Treating infected cells with SR9009 limits viral replication and secretion of infectious particles, showing that post-entry steps in the viral life cycle are influenced by the circadian system. Our study suggests new approaches to understand and improve therapeutic targeting of COVID-19 MESHD.

    SARS-CoV-2 Nsp5 HGNC Protein Causes Acute Lung Inflammation MESHD: A Dynamical Mathematical Model

    Authors: José Díaz; Elena R. Álvarez-Buylla; Antonio Bensussen

    id:10.20944/preprints202012.0749.v2 Date: 2021-03-15 Source:

    In the present work we propose a dynamical mathematical model of the lung cells inflammation process MESHD in response to SARS-CoV-2 infection MESHD. In this scenario the main protease PROTEIN Nsp5 HGNC enhances the inflammatory process, increasing the levels of NF kB, IL-6 HGNC, Cox2 HGNC, and PGE2 with respect to a reference state without the virus. In presence of the virus the translation rates of NF kB and IkB arise to a high constant value, and when the translation rate of IL-6 HGNC also increases above the threshold value of 7 pg mL-1 s-1 the model predicts a persistent over stimulated immune state with high levels of the cytokine IL-6 HGNC. Our model shows how such over stimulated immune state becomes autonomous of the signals from other immune cells such as macrophages and lymphocytes, and does not shut down by itself. We also show that in the context of the dynamical model presented here, Dexamethasone or Nimesulide have little effect on such inflammation MESHD state of the infected lung cell, and the only form to suppress it is with the inhibition of the activity of the viral protein Nsp5 HGNC.To that end, our model suggest that drugs like Saquinavir may be useful. In this form, our model suggests that Nsp5 HGNC is effectively a central node underlying the severe acute lung inflammation MESHD during SARS-CoV-2 infection MESHD. The persistent production of IL-6 HGNC by lung cells can be one of the causes of the cytokine storm observed in critical patients with COVID19 MESHD. Nsp5 HGNC seems to be the switch to start inflammation MESHD, the consequent overproduction of the ACE2 HGNC receptor, and an important underlying cause of the most severe cases of COVID19 MESHD.

    An update of coronavirus disease 2019 MESHD ( COVID-19 MESHD): an essential brief for clinicians

    Authors: Afshin Zare; Seyyede Fateme Sadati-Seyyed-Mahalle; Amirhossein Mokhtari; Nima Pakdel; Zeinab Hamidi; Sahar Almasi-Turk; Neda Baghban; Arezoo Khoradmehr; Iraj Nabipour; Mohammad Amin Behzadi; Amin Tamadon

    id:10.20944/preprints202102.0530.v1 Date: 2021-02-23 Source:

    During 2019, the number of patients suffering from cough, fever MESHD and reduction of WBC’s count increased. At the beginning, this mysterious illness was called “ fever MESHD with unknown origin”. At the present time, the cause of this pneumonia MESHD is known as the 2019 novel coronavirus (2019-nCoV) or the severe acute respiratory syndrome MESHD corona virus 2 (SARS-CoV-2). The SARS-CoV-2 is one member of great family of coronaviruses. Coronaviruses can cause different kind of illnesses including respiratory, enteric, hepatic, and neurological diseases MESHD in animals like cat and bat. Coronaviruses are enveloped positive-stranded RNA viruses. The SARS-CoV-2 has some particular structures for binding to host cells, reproducing itself in cells and damaging human cells. The SARS-CoV-2 can bind angiotensin-converting enzyme 2 HGNC ( ACE‐2 HGNC) receptors and cause various difficulties for human. The SARS-CoV-2 can cause either not-serious issues like fever MESHD and cough MESHD or serious concerns such as multi-organ failure MESHD. Source(s) of SARS-CoV-2 is under debate. Malayan pangolin and bat are the most suspicious candidate for being sources of the SARS-CoV-2. The SARS-CoV-2 can be transmitted by various ways such as transmitting from infected human to healthy human and can make severe pneumonia MESHD, which can lead to death. The SARS-CoV-2 can infect different kind of people with different ages, races, and social and economic levels. The SARS‐CoV‐2 infection MESHD can cause various sorts of clinical manifestations like cough and fever MESHD and intensity of signs and symptoms depends on sufferer conditions. Clinicians use all of available documents and tests like laboratory, histopathological and radiological findings for diagnosing new cases and curing patients with high accuracy. At the present time, there is no particular way for treating SARS-CoV-2 infection MESHD; neither antiviral drugs nor palliative agents. It seems that the best way for standing against the SARS-CoV-2 infection MESHD is preventing from it by social distancing and vaccination. This review tries to prepare an essential brief update about SARS-CoV-2 infection MESHD for clinicians.

    Full Brain and Lung Prophylaxis against SARS-CoV-2 by Intranasal Lentiviral Vaccination in a New hACE2 HGNC Transgenic Mouse Model or Golden Hamsters

    Authors: Min-Wen Ku; Pierre Authie; Maryline Bourgine; Francois Anna; Amandine Noirat; Fanny Moncoq; Benjamin Vesin; Fabien Nevo; Jodie Lopez; Philippe Souque; Catherine Blanc; Sebastien Chardenoux; Ilta Lafosse; David Hardy; Kirill Nemirov; Francoise Guinet; Francina Langa Vives; Laleh Majlessi; Pierre Charneau

    doi:10.1101/2021.02.03.429211 Date: 2021-02-03 Source: bioRxiv

    Non-integrative, non-cytopathic and non-inflammatory lentivectors are particularly suitable for mucosal vaccination and recently emerge as a promising strategy to elicit sterilizing prophylaxis against SARS-CoV-2 in preclinical animal models. Here, we demonstrate that a single intranasal administration of a lentivector encoding a prefusion form of SARS-CoV-2 spike PROTEIN glycoprotein induces full protection of respiratory tracts and totally avoids pulmonary inflammation MESHD in the susceptible hamster model. More importantly, we generated a new transgenic mouse strain, expressing the human Angiotensin Converting Enzyme 2 HGNC, with unprecedent brain permissibility to SARS-CoV-2 replication and developing a lethal disease in <4 days post infection. Even though the neurotropism of SARS-CoV-2 MESHD is now well established, so far other vaccine strategies under development have not taken into account the protection of central nervous system. Using our highly stringent transgenic model, we demonstrated that an intranasal booster immunization with the developed lentivector vaccine candidate achieves full protection of both respiratory tracts and central nervous system against SARS-CoV-2.

    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

    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.

    Genetic variability in COVID-19 MESHD-related genes in the Brazilian population

    Authors: Rodrigo Secolin; Tania K de Araujo; Marina C. Gonsales; Cristiane S. Rocha; Michel Satya Naslavsky; Luiz De Marco; Maria Bicalho; Vinicius L Vazquez; Mayana Zatz; Wilson A Silva Jr.; Iscia Lopes-Cendes; Sebla B Kutluay; Mei-Ling Li; Gary Brewer; Blanton S Tolbert; Amanda E Hargrove; Alexandra W. Dretler; Ria Gripaldo; Andrea N. Lane; Hao Wu; Saeyun Lee; Mindy Hernandez; Vanessa Engineer; John Varghese; Sang Le; Iñaki Sanz; John L. Daiss; Frances Eun-Hyung Lee

    doi:10.1101/2020.12.04.411736 Date: 2020-12-06 Source: bioRxiv

    SARS-CoV-2 employs the angiotensin-converting enzyme 2 HGNC ( ACE2 HGNC) receptor and the transmembrane serine protease ( TMPRSS2 HGNC) to infect human lung cells. Previous studies have suggested that different host genetic backgrounds in ACE2 HGNC and TMPRSS2 HGNC could contribute to differences in the rate of infection or severity of COVID-19 MESHD. Recent studies also showed that variants in 15 genes related to type I interferon immunity to influenza virus could predispose to life-threatening COVID-19 MESHD pneumonia MESHD. Additional genes ( SLC6A20 HGNC, LZTFL1 HGNC, CCR9 HGNC, FYCO1 HGNC, CXCR6 HGNC, XCR1 HGNC, IL6 HGNC, CTSL HGNC, ABO, and FURIN HGNC) and HLA alleles have also been implicated in response to infection with SARS-CoV-2. Currently, Brazil has recorded the third-highest number of COVID-19 MESHD patients worldwide. We aim to investigate the genetic variation present in COVID-19 MESHD-related genes in the Brazilian population. We analysed 27 candidate genes and HLA alleles in 954 admixed Brazilian exomes. We used the information available in two public databases ( and, and additional exomes from individuals born in southeast Brazil, the region with the highest number of COVID-19 MESHD patients in the country. Variant allele frequencies were compared with the 1000 Genomes Project phase 3 (1KGP) and the gnomAD databases. We found 395 non-synonymous variants; of these, 325 were also found in the 1000 Genome Project phase 3 (1KGP) and/or gnomAD. Six of these variants were previously reported as putatively influencing the rate of infection or clinical prognosis for COVID-19 MESHD. The remaining 70 variants were identified exclusively in the Brazilian sample, with a mean allele frequency of 0.0025. In silico prediction of the impact in protein function revealed that three of these rare variants were pathogenic. Furthermore, we identified HLA alleles that were previously associated with COVID-19 MESHD response at loci DQB1 HGNC and DRB1 HGNC. Our results showed genetic variability common to other populations, but also rare and ultra-rare variants exclusively found in the Brazilian population. These findings could potentially lead to differences in the rate of infection or response to infection by SARS-CoV-2 and should be further investigated in patients with the disease.

    A SARS-CoV-2 neutralizing antibody selected from COVID-19 MESHD patients by phage display is binding to the ACE2 HGNC-RBD interface and is tolerant to known RBD mutations

    Authors: Federico Bertoglio; Viola Fühner; Maximilian Ruschig; Philip Alexander Heine; Ulfert Rand; Thomas Klünemann; Doris Meier; Nora Langreder; Stephan Steinke; Rico Ballmann; Kai-Thomas Schneider; Kristian Daniel Ralph Roth; Philipp Kuhn; Peggy Riese; Dorina Schäckermann; Janin Korn; Allan Koch; Susanne Zock-Emmenthal; Marlies Becker; Margitta Scholz; Gustavo Marçal Schmidt Garcia Moreira; Esther Veronika Wenzel; Giulio Russo; Hendrikus S.P. Garritsen; Sebastian Casu; Andreas Gerstner; Günter Roth; Andreas Hermann; Thomas Schirrmann; Stefan Dübel; André Frenzel; Joop Van den Heuvel; Luka Cicin-Sain; Maren Schubert; Michael Hust

    doi:10.1101/2020.12.03.409318 Date: 2020-12-03 Source: bioRxiv

    The novel betacoranavirus SARS-CoV-2 causes a form of severe pneumonia disease MESHD, termed COVID-19 MESHD ( coronavirus disease 2019 MESHD). Recombinant human antibodies are proven potent neutralizers of viruses and can block the interaction of viral surface proteins with their host receptors. To develop neutralizing anti-SARS-CoV-2 antibodies, antibody gene libraries from convalescent COVID-19 MESHD patients were constructed and recombinant antibody fragments (scFv) against the receptor binding domain (RBD) of the S1 subunit of the viral spike (S) protein PROTEIN were selected by phage display. The selected antibodies were produced in the scFv-Fc format and 30 showed more than 80% inhibition of spike (S1-S2) binding to cells expressing ACE2, assessed by flow cytometry screening assay. The majority of these inhibiting antibodies are derived from the VH3-66 V-gene. The antibody STE90-C11 showed an IC50 of 0.56 nM in a plaque-based live SARS-CoV-2 neutralization assay. The crystal structure of STE90-C11 in complex with SARS-CoV-2-RBD was solved at 2.0 A resolution showing that the antibody binds at the same region as ACE2 to RBD. In contrast to other published anti-SARS-CoV-2 antibodies, the binding of STE90-C11 is not blocked by known RBD mutations, endowing our antibody with higher intrinsic resistance to those possible escape mutants.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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