Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (49)

NSP5 (6)

ComplexRdRp (4)

ProteinN (3)

ProteinE (3)


SARS-CoV-2 Proteins
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    SARS-COV-2 antibody prevalence in patients on dialysis in the US in January 2021

    Authors: Shuchi Anand; Maria Montez-Rath; Jialin Han; LinaCel Cadden; Patti Hunsader; Russell Kerschmann; Paul Beyer; Scott D Boyd; Pablo Garcia; Mary Dittrich; Geoffery A Block; Julie Parsonnet; Glenn M Chertow

    doi:10.1101/2021.03.07.21252786 Date: 2021-03-09 Source: medRxiv

    Background: To estimate seroprevalence of SARS-CoV-2 antibodies in the US, the country with largest absolute numbers of COVID19 MESHD cases and deaths MESHD in the world, we conducted a cross-sectional assessment from a sample of patients receiving dialysis in January 2021. Methods: We tested remainder plasma of 21,424 patients receiving dialysis through the third-largest US dialysis organization, with facilities located nationwide. We used the Siemens spike protein PROTEIN receptor binding domain total antibody assay to estimate crude SARS-CoV-2 seroprevalence, and then estimated seroprevalence for the US dialysis and adult population by standardizing by age, sex and region. We also compared January 2021 seroprevalence and case-detection rates to that from a similar subsample of patients receiving dialysis who had been tested in July 2020. Results: Patients in the sample were disproportionately from older age and minority race/ethnic groups. Seroprevalence of SARS-CoV-2 was 18.9% (95% CI: 18.3-19.5%) in the sample, 18.7% (18.1-19.2%) standardized to the US dialysis population, and 21.3% (20.3-22.3%) standardized to the US adult population (range 15.3-20.8% in the Northeast and South respectively). Younger age groups (18-44 years), and persons self-identifying as Hispanic or living in Hispanic neighborhoods, and persons living in the poorest neighborhoods were among the subgroups with the highest seroprevalence (25.9% (24.1-27.8%), 25.1% (23.6-26.4%), 24.8% (23.2-26.5%) respectively). Compared to data from July 2020, we observed diminished variability in seroprevalence by geographic region and urban-rural status. Estimated case detection rate increased from 14% to 23% in July 2020 to January 2021. Conclusions: A year after the first case of SARS-CoV-2 infection MESHD was detected in the US, fewer than one in four adults have evidence of SARS-CoV-2 antibodies. Vaccine roll out to majority minority neighborhoods and poorer neighborhoods will be critical to disrupting the spread of infection.

    Pyroptosis of syncytia formed by fusion of SARS-CoV-2 Spike PROTEIN SARS-CoV-2 Spike MESHD and ACE2 HGNC expressing cells

    Authors: Huabin Ma; Zhoujie Zhu; Huaipeng Lin; Shanshan Wang; Peipei Zhang; Yanguo Li; Long Li; Jinling Wang; Yufen Zhao; Jiahuai Han

    doi:10.1101/2021.02.25.432853 Date: 2021-02-25 Source: bioRxiv

    SARS-Cov-2 infected cells fused with the ACE2 HGNC-positive neighboring cells forming syncytia. However, the effect of syncytia in disease development is largely unknown. We established an in vitro cell-cell fusion system and used it to mimic the fusion of SARS-CoV-2 infected MESHD cells with ACE2 HGNC-expressing cells to form syncytia. We found that Caspase-9 HGNC was activated after syncytia formation, and Caspase-3/7 was activated downstream of Caspase-9 HGNC, but it triggered GSDME-dependent pyroptosis rather than apoptosis. What is more, single cell RNA-sequencing data showed that both ACE2 HGNC and GSDME were expression in alveolar type MESHD 2 cells in human lung. We propose that pyroptosis is the fate of syncytia formed by SARS-CoV-2 infected host MESHD cells and ACE2 HGNC-positive cells, which indicated that lytic death of syncytia MESHD may contribute to the excessive inflammatory responses in severe COVID-19 MESHD patients.

    Conserved in 186 Countries The RBD Fraction of SARS CoV-2 S-Protein PROTEIN With in-Silico T500S Mutation Strongly Blocks ACE2 Rejecting The Viral Spike; A Molecular-Docking Analysis.

    Authors: Amrita Banerjee; Mehak Kanwar; Dipannita Santra; Smarajit Maiti

    doi:10.21203/ Date: 2021-02-20 Source: ResearchSquare

    SARS CoV-2 developed a global pandemic with millions of infections/deaths MESHD. The role of blocker/inhibitor of ACE2 and viral-spikes Receptor-Binding-Domain RBD-blockers has been reported. In the current study, conserved RBD portions or cuts from 186 countries were screened and compared with WUHAN-Hu-1 wild-type by CLUSTAL X2 and Structural alignment analyses using Pymol. The RBD of ACE2 bound nCOV2 crystal-structure (2.68 Å) 6VYB1 was analyzed by PyMol and compared with RBD-Cut docking by Haddock and Patch Dock. Extensive structural study/trial to introduce point/double/triple mutations in the following locations (Y489S/Y453S/T500S/T500Y)/ (Y489S,Y453S/Y489S,T500S/Y489S,T500Y/Y453S,T500S/Y453S,T500Y)/ (Y489S,Y453S,T500S/ Y489S,Y453S,T500Y) of CUT4 were tested with Swiss Model Expacy. Blind docking of mutated CUTs to ACE2 (6VW1) by Haddock and Hawkdock was performed and complete rejection of nCOV2 was optimized through its re-docking trial and using pre-docked ACE2. Further, competitive-docking was performed and its binding analyses were done by PRODIGY. Present results suggest that compared to the wild-spike, CUT4 showed extra LYS31-PHE490 and GLN42-GLN498 bonding and lack of TYR41-THR500 interaction (in wild H-bond: 2.639Å) with ACE2 RBD, which can potentially but compete with the wild-spike. Whereas mutated CUT4 strongly binds with the ACE2 RBD, promoting TYR41-T500S (H-bond: 2.0Å and 1.8Å)/T500Y (H-bond: 2.6Å) interaction and complete inhibition of ACE2 RBD-nCOV2 S-protein PROTEIN binding. Mutant combinations T500S, Y489S,T500S and Y489S,Y453S,T500Y were found to be the most potent blocker of ACE2. It is hypothesized that Cut4 mutant is kinetically more favoured for ACE2-RBD binding and even reject whole glycosylated nCoV2 in all format of experiments; pre-dock, post-dock, and competitive-docking. Studies are necessary in this regard.

    SARS-CoV-2 variant evolution in the United States: High accumulation of viral mutations over time likely through serial Founder Events and mutational bursts.

    Authors: Rafail Nikolaos Tasakis; Georgios Samaras; Anna Jamison; Michelle Lee; Alexandra Paulus; Gabrielle Whitehouse; Laurent Verkoczy; F. Nina Papavasiliou; Marilyn Diaz

    doi:10.1101/2021.02.19.431311 Date: 2021-02-19 Source: bioRxiv

    Since the first case of COVID-19 MESHD in December 2019 in Wuhan, China, SARS-CoV-2 has spread worldwide and within a year has caused 2.29 million deaths globally. With dramatically increasing infection numbers, and the arrival of new variants with increased infectivity, tracking the evolution of its genome is crucial for effectively controlling the pandemic and informing vaccine platform development. Our study explores evolution of SARS-CoV-2 in a representative cohort of sequences covering the entire genome in the United States, through all of 2020 and early 2021. Strikingly, we detected many accumulating Single Nucleotide Variations (SNVs) encoding amino acid changes in the SARS-CoV-2 genome, with a pattern indicative of RNA editing enzymes as major mutators of SARS-CoV-2 genomes. We report three major variants through October of 2020. These revealed 14 key mutations that were found in various combinations among 14 distinct predominant signatures. These signatures likely represent evolutionary lineages of SARS-CoV-2 in the U.S. and reveal clues to its evolution such as a mutational burst in the summer of 2020 likely leading to a homegrown new variant, and a trend towards higher mutational load among viral isolates, but with occasional mutation loss. The last quartile of 2020 revealed a concerning accumulation of mostly novel low frequency replacement mutations in the Spike protein PROTEIN, and a hypermutable glutamine residue near the putative furin cleavage site. Finally, the end of the year data revealed the presence of known variants of concern including B.1.1.7, which has acquired additional Spike mutations. Overall, our results suggest that predominant viral sequences are dynamically evolving over time, with periods of mutational bursts and unabated mutation accumulation. This high level of existing variation, even at low frequencies and especially in the Spike-encoding region may be become problematic when superspreader events, akin to serial Founder Events in evolution, drive these rare mutations to prominence. AUTHOR SUMMARYThe pandemic of coronavirus disease 2019 MESHD ( COVID-19 MESHD), caused by the severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), has caused the death MESHD of more than 2.29 million people and continues to be a severe threat internationally. Although simple measures such as social distancing, periodic lockdowns and hygiene protocols were immediately put into force, the infection rates were only temporarily minimized. When infection rates exploded again new variants of the virus began to emerge. Our study focuses on a representative set of sequences from the United States throughout 2020 and early 2021. We show that the driving force behind the variants of public health concern, is widespread infection and superspreader events. In particular, we show accumulation of mutations over time with little loss from genetic drift, including in the Spike region, which could be problematic for vaccines and therapies. This lurking accumulated genetic variation may be a superspreader event from becoming more common and lead to variants that can escape the immune protection provided by the existing vaccines.

    Variation analysis of SARS-CoV-2 complete sequences from Iran

    Authors: Jale Moradi; Mohsen Moghoofei; Amir Houshang Alvandi; Ramin Abiri; Oladapo Oyebode; Yongli Wang; Jun Su; Huanxin Su; Evandro Fei Fang; ZhangJing Zhang; Jikai Zhang; Oscar Junhong Luo; Pengchen Wang; Guobing Chen

    doi:10.1101/2021.01.23.427885 Date: 2021-01-24 Source: bioRxiv

    The SARS-CoV-2 is a new emerging coronavirus initially reported in China in late December 2019 and rapidly spread to the whole of the world. To date, 1261903 total cases and 55830 deaths MESHD are reported from Iran as of 8 January. In this study, we investigated all the complete sequences of SARS-CoV-2 that publicly reported from Iran. Twenty-four sequences between March to September 2020 were analyzed to identify genome variations and phylogenetic relationships. Furthermore, we assessed the amino acid changes related to the spike glycoprotein PROTEIN as an important viral factor associated with the entry to the host cells and as a vaccine target. Most of the variations occur in the ORF1ab PROTEIN, S, N, intergenic, and ORF7 regions. The analysis of spike protein PROTEIN mutations demonstrated that the D614G mutation could be detected from May and beyond. Phylogenetic analysis showed that most of the circulated viruses in Iran are belong to the B.4 lineage. Although, we found a limited number of variants associated with the B.1 lineage carrying D614G mutation. Furthermore, we detected a variant characterize as the B.1.36 lineage with sixteen mutations in the spike protein PROTEIN region. This study showed the frequency of the viral populations in Iran as of September, therefore, there is an emergent need for genomic surveillance to track viral lineage shift in the country beyond September. These data would help to predict the future situation and apply better strategies to control the pandemic.

    Potent Inhibition of Severe Acute Respiratory Syndrome Coronavirus 2 MESHD (SARS-CoV-2) by photosensitizers

    Authors: Shujuan Yu; Gaohui Sun; Yaqun Sui; Hanlin Li; Ning Zhang; Yuhai Bi; George Gao; Longguang Jiang; Peng Xu; Cai Yuan; Yang Yang; Mingdong Huang

    doi:10.21203/ Date: 2021-01-22 Source: ResearchSquare

    The pandemic of coronavirus disease 2019 MESHD ( COVID-19 MESHD) caused by severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2) has exploded since December 2019, and causes more than 2 million death MESHD with more than 95 million people infected as of Jan. 21th, 2021 globally1,2. Angiotensin-converting enzyme 2 HGNC ( ACE2 HGNC), expressed in the lungs, arteries, heart, kidney, intestines, and nasal epithelium3, has been shown to be the primary entry point targeted by the surface spike protein PROTEIN of SARS-CoV-2. Currently, no proven antiviral treatment for SARS-CoV-2 infection MESHD is available. In this study, we screened a number of photosensitizers for photodynamic viral inactivation, and found compounds pentalysine β-carbonylphthalocyanine zinc (ZnPc5K) and chlorin e6 (ce6) potently inhibited the viral infection and replication in vitro with half-maximal effective concentrations (EC50) values at nanomolar level. Such viral inactivation strategy is implementable, and has unique advantages, including resistance to virus mutations, affordability compared to the monoclonal antibodies, and lack of long-term toxicity MESHD.

    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.

    The SARS-CoV-2 spike PROTEIN protein disrupts the cooperative function of human cardiac pericytes - endothelial cells through CD147 HGNC receptor-mediated signalling: a potential non-infective mechanism of COVID-19 MESHD microvascular disease

    Authors: Elisa Avolio; Monica Gamez; Kapil Gupta; Rebecca Foster; Imre Berger; Massimo Caputo; Andrew D. Davidson; Darryl Hill; Paolo Madeddu; Shawn A Abbasi; Whitney Pickens; Katia George; Daniel R Boutz; Dalton M Towers; Jonathan R McDaniel; Daniel Billick; Jule Goike; Lori Rowe; Dhwani Batra; Jan Pohl; Justin Lee; Shivaprakash Gangappa; Suryaprakash Sambhara; Michelle Gadush; Nianshuang Wang; Maria D Person; Brent L Iverson; Jimmy D Gollihar; John Dye; Andrew Herbert; Ralph S Baric; Jason S McLellan; George Georgiou; Jason J Lavinder; Gregory C Ippolito; Fergus Gleeson; Yper Hall; Simon G. P. Funnell; Sally Sharpe; Francisco Javier Salguero; Andrew R Gorringe; Miles Carroll

    doi:10.1101/2020.12.21.423721 Date: 2020-12-21 Source: bioRxiv

    Background: Severe coronavirus disease 2019 MESHD ( COVID-19 MESHD) manifests as a life-threatening microvascular syndrome MESHD. The severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2) uses primarily the capsid spike (S) protein PROTEIN to engage with its receptors and infect host cells. To date, it is still not known if the S protein PROTEIN alone, without the other viral elements, is able to trigger vascular cell signalling and provoke cell dysfunction. Methods: We investigated the effects of the recombinant, stabilised S protein PROTEIN on primary human cardiac pericytes (PCs) signalling and function. Endpoints included cell viability, proliferation, migration, cooperation with endothelial cells (ECs) in angiogenesis assays, and release of pro-inflammatory cytokines. Adopting a blocking strategy against the S protein PROTEIN receptors ACE2 HGNC and CD147 HGNC, we explored which receptor mediates the S protein PROTEIN signalling in PCs. Findings: We show, for the first time, that the recombinant S protein PROTEIN alone elicits functional alterations in cardiac PCs. This was documented as: (1) increased migration, (2) reduced ability to support EC network formation on Matrigel, (3) secretion of pro-inflammatory molecules typically involved in the cytokine storm; and (4) production of pro-apoptotic factors responsible for EC death MESHD. Furthermore, the S protein PROTEIN stimulates the phosphorylation/activation of the extracellular signal-regulated kinase 1/2 HGNC (ERK1/2) through the CD147 HGNC receptor, but not ACE2 HGNC, in cardiac PCs MESHD. Accordingly, the neutralization of CD147 HGNC, using a blocking antibody, prevented the activation of ERK1/2 and partially rescued the PC function in the presence of the S protein PROTEIN. Interpretation: Our findings suggest the new, intriguing hypothesis that the S protein PROTEIN may elicit vascular cell dysfunction MESHD, potentially amplifying, or perpetuating, the damage caused by the whole coronavirus. This mechanism may have clinical and therapeutic implication.

    pH and Receptor Induced Confirmational Changes- Implications Towards S1 Dissociation of SARS-CoV2 Spike Glycoprotein PROTEIN

    Authors: Jesu E. Castin; Daniel A. Gideon; Karthik S Sudarsha; Sherlin A Rosita; Imre Berger; Massimo Caputo; Andrew D. Davidson; Darryl Hill; Paolo Madeddu; Shawn A Abbasi; Whitney Pickens; Katia George; Daniel R Boutz; Dalton M Towers; Jonathan R McDaniel; Daniel Billick; Jule Goike; Lori Rowe; Dhwani Batra; Jan Pohl; Justin Lee; Shivaprakash Gangappa; Suryaprakash Sambhara; Michelle Gadush; Nianshuang Wang; Maria D Person; Brent L Iverson; Jimmy D Gollihar; John Dye; Andrew Herbert; Ralph S Baric; Jason S McLellan; George Georgiou; Jason J Lavinder; Gregory C Ippolito; Fergus Gleeson; Yper Hall; Simon G. P. Funnell; Sally Sharpe; Francisco Javier Salguero; Andrew R Gorringe; Miles Carroll

    doi:10.1101/2020.12.21.410357 Date: 2020-12-21 Source: bioRxiv

    Viruses, being obligate intracellular parasites, must first attach themselves and gain entry into host cells. Viral fusion machinery is the central player in the viral attachment process in almost every viral disease. Viruses have incorporated an array of efficient fusion proteins on their surfaces to bind efficiently to host cell receptors. They make use of the host proteolytic enzymes to rearrange their surface protein(s PROTEIN) into the form which facilitates their binding to host-cell membrane proteins and subsequently, fusion. This stage of viral entry is very critical and has many therapeutic implications. The current global pandemic of COVID-19 MESHD has sparked severe health crisis and economic shutdowns. SARS-CoV2, the etiological agent of the disease has led to millions of deaths MESHD and brought the scientific community together in an attempt to understand the mechanisms of SARS-CoV2 pathogenesis and mortality. Like other viral fusion machinery, CoV2 spike ( S) glycoprotein PROTEIN- 'The Demogorgon' poses the same questions about viral-host cell fusion. The intermediate stages of S protein PROTEIN-mediated viral fusion are unclear owing to the lack of structural insights and concrete biochemical evidence. The mechanism of conformational transition is still unclear. S protein PROTEIN binding and fusion with host cell receptors, Eg., angiotensin-converting enzyme-2 ( ACE2 HGNC) is accompanied by cleavage of S1/S2 subunits. To track the key events of viral-host cell fusion, we have identified (in silico) that low pH-induced conformational change and ACE-2 HGNC binding events promote S1 dissociation. Deciphering key mechanistic insights of SARS-CoV2 fusion will further our understanding of other class- I fusion proteins.

    SARS-CoV-2 spike PROTEIN protein interacts with and activates TLR4

    Authors: Yingchi Zhao; Ming Kuang; Xiangxi Wang; Fuping You; Ruoxi Pi; Giovanny J. Martinez-Colon; Thanmayi Ranganath; Nancy Q. Zhao; Shalina Taylor; Winston Becker; - Stanford COVID-19 Biobank; David Jimenez-Morales; Andra L. Blomkalns; Euan A. Ashley; Kari C. Nadeau; Samuel Yang; Susan Holmes; Marlene Rabinovitch; Angela J. Rogers; William J. Greenleaf; Catherine A. Blish; Yoshiharu Matsuura; Daron M Standley; Tatsuo Shioda; Hisashi Arase; John Booth; Silvano Bosari; Florence T Bourgeois; Nicholas W Brown; Luca Chiovato; Lorenzo Chiudinelli; Arianna Dagliati; Batsal Devkota; Robert W Follett; Thomas Ganslandt; Noelia García Barrio; Tobias Gradinger; Romain Griffier; David A Hanauer; John H Holmes; Petar Horki; Kenneth M Huling; Richard W Issitt; Vianney Jouhet; Mark S Keller; Detlef Kraska; Molei Liu; Yuan Luo; Alberto Malovini; Kenneth D Mandl; Chengsheng Mao; Anupama Maram; Thomas Maulhardt; Bucalo Mauro; Marianna Milano; Jason H Moore; Jeffrey S Morris; Michele Morris; Danielle L Mowery; Thomas P Naughton; Kee Yuan Ngiam; James B Norman; Lav P Patel; Miguel Pedrera Jimenez; Emily R Schriver; Luigia Scudeller; Neil J Sebire; Pablo Serrano Balazote; Anastasia Spiridou; Amelia LM Tan; Byorn W.L. Tan; Valentina Tibollo; Carlo Torti; Enrico M Trecarichi; Maria Trecarichi; Michele Vitacca; Alberto Zambelli; Chiara Zucco; - Consortium for Clinical Characterization of COVID-19 by EHR; Isaac S Kohane; Tianxi Cai; Gabriel A Brat

    doi:10.1101/2020.12.18.423427 Date: 2020-12-18 Source: bioRxiv

    The onset of sepsis MESHD is an important feature of COVID19 MESHD and a main cause of death MESHD. It is unknown how SARS-CoV-2 infection MESHD results in viral sepsis MESHD in human. We recently found that SARS-CoV-2 provoked an anti-bacterial like response and activation of TLR4 HGNC pathway at the very early stage of infection in animal models. This abnormal immune response led to emergency granulopoiesis and sepsis MESHD. However, the original trigger of TLR4 HGNC signaling by SARS-CoV-2 is unknown. We here identified that the trimeric spike protein PROTEIN of SARS-CoV-2 could bind to TLR4 HGNC directly and robustly activate downstream signaling in monocytes and neutrophils. Moreover, specific TLR4 HGNC or NFKB inhibitor, or knockout of MyD88 HGNC could significantly block IL-1B HGNC induction by spike protein PROTEIN. We thus reveal that spike protein PROTEIN of SARS-CoV-2 functions as a potent stimulus causing TLR4 HGNC activation and sepsis MESHD related abnormal responses.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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