Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (100)

NSP5 (7)

ProteinN (4)

ComplexRdRp (4)

ProteinE (2)


SARS-CoV-2 Proteins
    displaying 161 - 170 records in total 187
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    Neuroinvasive Potential of A Primary Respiratory Pathogen SARS-CoV2: Exploring the Underrecognized

    Authors: Durjoy Lahiri; Ritwick Mondal; Shramana Deb; Deebya Bandopadhyay; Gourav Shome; Sukanya Sarkar; Subhas C. Biswas

    id:10.20944/preprints202004.0382.v1 Date: 2020-04-21 Source:

    After the emergence of Severe Acute Respiratory Syndrome Coronavirus(SARS-CoV) and Middle East Respiratory Syndrome Coronavirus (MERS-CoV MESHD) in the last two decades, the world is facing its new challenge in SARS-CoV-2 pandemic with unfathomable global responses. The characteristic clinical symptoms for Coronavirus ( COVID-19 MESHD) affected patients are high fever, dry-cough, dyspnoea MESHD, lethal pneumonia MESHD whereas some patients also show few additional neurological signs such as headache MESHD, nausea MESHD, vomiting MESHD. The accumulative evidences suggest that Coronavirus is not only confined within the respiratory tract and that may also invade in central nervous system (CNS), peripheral nervous system (PNS) inducing some fatal Neurological diseases MESHD. Here we analyse the phylogenetic perspective of SARS-CoV2 with other strains of β-Coronaviridae from a standpoint of neurological spectrum disorders MESHD. Based on the existing case reports, literature and open data-bases, we also analyse the differential distribution of neurological impairments MESHD in COVID-19 MESHD positive patients along with angiotensin-converting enzyme-2 HGNC( ACE2 HGNC) expression dynamics in neuronal and non-neuronal tissue of central and peripheral nervous system. Besides, we discuss the need for modulations in clinical approach from a neurological point of view, as a measure towards reducing disease transmission, morbidity and mortality in SARS-CoV2 positive patients.

    Broad Host Range of SARS-CoV-2 Predicted by Comparative and Structural Analysis of ACE2 HGNC in Vertebrates

    Authors: Joana Damas; Graham M. Hughes; Kathleen C. Keough; Corrie A. Painter; Nicole S. Persky; Marco Corbo; Michael Hiller; Klaus-Peter Koepfli; Andreas R. Pfenning; Huabin Zhao; Diane P. Genereux; Ross Swofford; Katherine S. Pollard; Oliver A. Ryder; Martin T. Nweeia; Kerstin Lindblad-Toh; Emma C. Teeling; Elinor K. Karlsson; Harris A. Lewin

    doi:10.1101/2020.04.16.045302 Date: 2020-04-18 Source: bioRxiv

    The novel coronavirus SARS-CoV-2 is the cause of Coronavirus Disease MESHD-2019 ( COVID-19 MESHD). The main receptor of SARS-CoV-2, angiotensin I converting enzyme 2 HGNC ( ACE2 HGNC), is now undergoing extensive scrutiny to understand the routes of transmission and sensitivity in different species. Here, we utilized a unique dataset of 410 vertebrates, including 252 mammals, to study cross-species conservation of ACE2 HGNC and its likelihood to function as a SARS-CoV-2 receptor. We designed a five-category ranking score based on the conservation properties of 25 amino acids important for the binding between receptor and virus, classifying all species from very high to very low. Only mammals fell into the medium to very high categories, and only catarrhine primates in the very high category, suggesting that they are at high risk for SARS-CoV-2 infection MESHD. We employed a protein structural analysis to qualitatively assess whether amino acid changes at variable residues would be likely to disrupt ACE2 HGNC/SARS-CoV-2 binding, and found the number of predicted unfavorable changes significantly correlated with the binding score. Extending this analysis to human population data, we found only rare (<0.1%) variants in 10/25 binding sites. In addition, we observed evidence of positive selection in ACE2 HGNC in multiple species, including bats. Utilized appropriately, our results may lead to the identification of intermediate host species for SARS-CoV-2, justify the selection of animal models of COVID-19 MESHD, and assist the conservation of animals both in native habitats and in human care.

    Identification of SARS-CoV-2 Cell Entry Inhibitors by Drug Repurposing Using in Silico Structure-Based Virtual Screening Approach

    Authors: Shweta Choudhary; Yashpal S. Malik; Shailly Tomar

    doi:10.26434/chemrxiv.12005988.v2 Date: 2020-04-15 Source: ChemRxiv

    The rapidly spreading, highly contagious and pathogenic SARS-coronavirus MESHD 2 (SARS-CoV-2) associated Coronavirus Disease 2019 MESHD ( COVID-19 MESHD) has been declared as a pandemic by the World Health Organization (WHO). The novel 2019 SARS-CoV-2 enters the host cell by binding of the viral surface spike glycoprotein PROTEIN ( S-protein HGNC S-protein PROTEIN) to angiotensin converting enzyme 2 HGNC ( ACE2 HGNC). The virus specific molecular interaction with the host cell represents a promising therapeutic target for identifying SARS-CoV-2 antiviral drugs. The repurposing of drugs can provide a rapid and potential cure towards exponentially expending COVID-19 MESHD. Thereto, high-throughput virtual screening approach was used to investigate FDA approved LOPAC library drugs against both the S-protein HGNC S-protein PROTEIN and ACE2 HGNC host cell receptor. Primary screening identified a few promising drugs for both the targets, which were further analyzed in details by their binding energy, binding modes through molecular docking, dynamics and simulations. Evidently, Eptifibatide acetate, TNP, GNF5, GR 127935 hydrochloride hydrate and RS504393 were found binding to virus binding motifs of ACE2 HGNC receptor. Additionally, KT185, KT203 GSK1838705A, BMS195614, and RS504393 were identified to bind at the receptor binding site on the viral S-protein HGNC S-protein PROTEIN. These identified drug molecules may effectively assist in controlling the rapid spread of SARS-COV-2 by not only potentially inhibiting the virus at entry step but also as anti-inflammatory agents which could impart relief in lung injuries MESHD. Timely identification and determination of an effective drug to combat and tranquilize the COVID-19 MESHD global crisis is the utmost need of hour. Further, prompt in vivo testing to validate the anti-SARS-COV-2 inhibition by these drugs could save lives is justified.

    The Pathophysiology of Virulence of the COVID-19 MESHD

    Authors: Joseph De Soto; Shazia Hakim; Frederick Boyd

    id:10.20944/preprints202004.0077.v2 Date: 2020-04-15 Source:

    Background: On Dec 19, 2019, the public health department of China reported that an outbreak of pneumonia MESHD was caused by a novel Coronavirus. The virulence of the new virus COVID-19 MESHD was much greater than either the SARs and MERSs viruses and on March 11, 2020, the World Health Department (WHO) declared a worldwide pandemic. Understanding the pathophysiology of virulence of the SARS-COV-2 virus is absolutely necessary for understanding the transmission, virulence factors, reduce risk factors, clinical presentation, predict outcomes of the disease and provide guidance for any current or future treatment protocols. Methodology: A comprehensive PubMed search was performed during December 20, 2019 and April 03, 2020, utilizing the words: Wuhan Virus, COVID-19 MESHD, SARs coronavirus MESHD, ACE2, S-protein PROTEIN, virulence, clinical presentation, epidemiology, genome, treatment, structure, MERs, pathogenesis and/or pathology alone and in combination with other terms. Each paper was evaluated by three content experts for quality, reproducibility, credibility and reputation of the journal. Results: The SARS-COV-2 virus is much more virulent than either the SAR’s or MER’s virus and its ability to cause serious disease inversely corresponds to the person’s ability to produce T-cells which declines linearly with age. The ACE2 receptor binding site does not vary among different ethnic groups but do in ACE-2 HGNC expression levels. This variance in expression level may explain for different infectivity rates among men and women and predict and explain different susceptibilities to infection by different ethnic groups. Furthermore, by understanding the underlying pathophysiology one can explain and provide guidance to the clinical effectiveness of any treatment. Conclusions: The underlying pathophysiology of COVID-19 MESHD explains not only the virulence, and clinical presentation, but, explains at a molecular level the comorbidity risk factors such as hypertension MESHD, sex, and age. Ethnic and anatomic expression patterns of ACE-2 HGNC and associated pathophysiology suggests that Native Americans and Asians may be particularly susceptible to this disease.

    Myocyte Specific Upregulation of ACE2 HGNC in Cardiovascular Disease: Implications for SARS-CoV-2 mediated myocarditis

    Authors: Nathan R Tucker; Mark Chaffin; Kenneth C Bedi Jr.; Irinna Papangeli; Amer-Denis Akkad; Alessandro Arduini; Sikander Hayat; Gökcen Eraslan; Christoph Muus; Roby Bhattacharyya; Christian M Stegmann; - Human Cell Atlas Lung Biological Network; Kenneth B Margulies; Patrick T Ellinor

    doi:10.1101/2020.04.09.20059204 Date: 2020-04-14 Source: medRxiv

    Coronavirus disease 2019 MESHD ( COVID-19 MESHD) is a global pandemic caused by a novel severe acute respiratory syndrome coronavirus-2 MESHD (SARS-CoV-2). SARS-CoV-2 infection MESHD of host cells occurs predominantly via binding of the viral surface spike protein PROTEIN to the human angiotensin-converting enzyme 2 HGNC ( ACE2 HGNC) receptor. Hypertension MESHD and pre-existing cardiovascular disease MESHD are risk factors for morbidity from COVID-19 MESHD, and it remains uncertain whether the use of angiotensin converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARB) impacts infection MESHD and disease. Here, we aim to shed light on this question by assessing ACE2 HGNC expression in normal and diseased human myocardial samples profiled by bulk and single nucleus RNA-seq.

    Medical Basis for Increased Susceptibility of COVID-19 MESHD among the Navajo and other Indigenous Tribes

    Authors: Joseph De Soto; Shazia Hakim

    id:10.20944/preprints202004.0217.v1 Date: 2020-04-14 Source:

    Introduction The COVID-19 MESHD virus was initially reported in Dec 2019 as the causative agent of a pneumonia MESHD breakout in Wuhan China. This virus rapidly spread from China to Europe and the East Coast of the United States eventually reaching the South West United States and indigenous tribes in mid -March. Since, then the indigenous tribes have been devasted by the virus which the Governor of New Mexico has likened as an existential threat. Methodology A PubMed search was performed utilizing the words: Navajo Indian, Indigenous Indian, Wuhan Virus, COVID-19 MESHD, SARs coronavirus MESHD, A CE2, HGNC S protein PROTEIN, virulence, clinical presentation, epidemiology, genome, treatment, structure, MERs, pathogenesis and/or pathology alone and in combination with other terms. Each paper was evaluated by three content experts for quality, reproducibility, credibility and reputation of the journal Results: Navajo’s and other indigenous peoples may have elevated levels of A CE2 HGNCreceptors in their lungs and other tissues allowing greater susceptibility to the COVID-19 MESHD virus. Increased levels of diabetes MESHD and protein nutrition are directly related to increased morbidity and mortality in this group while obesity MESHD, COPD, and heart diseas are not. The increased morbidity and mortality is exasperated by an inability to test for COVID-19 MESHD Conclusion: The infectivity rate of Navaho’s on the reservation is 22 times higher than the national average with a death rate near 4%. Comorbidites account for some of the increased morbidity and mortality while lack of access to adequate health care unnecessarily magnifies the poor outcome. The threat to indigenous tribes in the Southwest of COVID-19 MESHD is dire.

    Human ACE2 HGNC receptor polymorphisms predict SARS-CoV-2 susceptibility

    Authors: Eric W Stawiski; Devan Diwanji; Kushal Suryamohan; Ravi Gupta; Frederic A Fellouse; Fah Sathirapongsasuti; Jiang Liu; Ying-Ping Jiang; Aakrosh Ratan; Monika Mis; Devi Santhosh; Sneha Somasekar; Sangeetha Mohan; Sameer Phalke; Boney Kuriakose; Aju Antony; Jagath R Junutula; Stephan C Schuster; Natalia Jura; Somasekar Seshagiri

    doi:10.1101/2020.04.07.024752 Date: 2020-04-10 Source: bioRxiv

    Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of coronavirus disease MESHD ( COVID-19 MESHD) that has resulted in a global pandemic. It is a highly contagious positive strand RNA virus and its clinical presentation includes severe to critical respiratory disease MESHD that appears to be fatal in [~]3-5% of the cases. The viral spike (S) coat protein engages the human angiotensin-converting enzyme2 HGNC ( ACE2 HGNC) cell surface protein to invade the host cell. The SARS-CoV-2 S-protein PROTEIN S-protein HGNC has acquired mutations that increase its affinity to human ACE2 HGNC by [~]10-15-fold compared to SARS-CoV S-protein MESHD S-protein PROTEIN S-protein HGNC, making it highly infectious. In this study, we assessed if ACE2 HGNC polymorphisms might alter host susceptibility to SARS-CoV-2 by affecting the ACE2 S-protein PROTEIN interaction. Our comprehensive analysis of several large genomic datasets that included over 290,000 samples representing >400 population groups identified multiple ACE2 HGNC protein-altering variants, some of which mapped to the S-protein PROTEIN S-protein HGNC-interacting ACE2 HGNC surface. Using recently reported structural data and a recent S-protein HGNC S-protein PROTEIN-interacting synthetic mutant map of ACE2 HGNC, we have identified natural ACE2 HGNC variants that are predicted to alter the virus-host interaction and thereby potentially alter host susceptibility. In particular, human ACE2 HGNC variants S19P, I21V, E23K, K26R, T27A, N64K, T92I, Q102P and H378R are predicted to increase susceptibility. The T92I variant, part of a consensus NxS/T N-glycosylation motif, confirmed the role of N90 glycosylation in immunity from non-human CoVs. Other ACE2 HGNC variants K31R, N33I, H34R, E35K, E37K, D38V, Y50F, N51S, M62V, K68E, F72V, Y83H, G326E, G352V, D355N, Q388L and D509Y are putative protective variants predicted to show decreased binding to SARS-CoV-2 S-protein PROTEIN S-protein HGNC. Overall, ACE2 HGNC variants are rare, consistent with the lack of selection pressure given the recent history of SARS-CoV MESHD epidemics, however, are likely to play an important role in altering susceptibility to CoVs.

    Type 2 and interferon inflammation strongly regulate SARS-CoV-2 related gene expression in the airway epithelium

    Authors: Satria P Sajuthi; Peter DeFord; Nathan D Jackson; Michael T Montgomery; Jamie L Everman; Cydney L Rios; Elmar Pruesse; James D Nolin; Elizabeth G Plender; Michael E Wechsler; Angel CY Mak; Celeste Eng; Sandra Salazar; Vivian Medina; Eric M Wohlford; Scott Huntsman; Deborah A Nickerson; Soren Germer; Michael C Zody; Goncalo Abecasis; Hyun Min Kang; Kenneth M Rice; Sam Oh; Jose Rodriguez-Santana; Esteban G Burchard; Max A Seibold

    doi:10.1101/2020.04.09.034454 Date: 2020-04-10 Source: bioRxiv

    Coronavirus disease 2019 MESHD ( COVID-19 MESHD) outcomes vary from asymptomatic infection to death. This disparity may reflect different airway levels of the SARS-CoV-2 receptor, ACE2 HGNC, and the spike protein PROTEIN activator, TMPRSS2 HGNC. Here we explore the role of genetics and co-expression networks in regulating these genes in the airway, through the analysis of nasal airway transcriptome data from 695 children. We identify expression quantitative trait loci (eQTL) for both ACE2 HGNC and TMPRSS2 HGNC, that vary in frequency across world populations. Importantly, we find TMPRSS2 HGNC is part of a mucus secretory network, highly upregulated by T2 inflammation MESHD through the action of interleukin-13 HGNC, and that interferon response to respiratory viruses highly upregulates ACE2 HGNC expression. Finally, we define airway responses to coronavirus infections MESHD in children, finding that these infections upregulate IL6 HGNC while also stimulating a more pronounced cytotoxic immune response relative to other respiratory viruses. Our results reveal mechanisms likely influencing SARS-CoV-2 infectivity MESHD and COVID-19 MESHD clinical outcomes.

    Genome Wide Analysis of Severe Acute Respiratory Syndrome Coronavirus-2 Implicates World-Wide Circulatory Virus Strains Heterogeneity

    Authors: M. Rafiul Islam; M. Nazmul Hoque; M. Shaminur Rahman; J. Akter Puspo; Masuda Akhter; Salma Akter; A. S. M. Rubayet-Ul-Alam; Munawar Sultana; Keith A. Crandall; M. Anwar Hossain

    id:10.20944/preprints202004.0137.v1 Date: 2020-04-09 Source:

    Severe acute respiratory syndrome coronavirus-2 MESHD (SARS-CoV-2), a novel evolutionarily divergent RNA virus etiological agent of COVID-19 MESHD, is responsible for present devastating pandemic respiratory illness MESHD. To explore the genomic signatures, we comprehensively analyzed 2,492 complete and/or near-complete genome sequences of SARS-CoV-2 strains reported from across the globe to the GISAID database up to 30 March 2020. Genome-wide annotations revealed 1,407 nucleotide-level mutations at different positions throughout the entire genome of SARS-CoV-2. Moreover, nucleotide deletion analysis found nine deletions throughout the genome, including in polyprotein (n=6), ORF10 PROTEIN (n=1) and 3´-UTR (n=2). Evidence from the systematic gene-level mutational and protein profile analyses revealed a large number of amino acid (aa) substitutions (n=722), making the viral proteins heterogeneous. Notably, residues of receptor-binding domain (RBD) having crucial interactions with angiotensin-converting enzyme 2 HGNC ( ACE2 HGNC), and cross-reacting neutralizing antibody were found to be conserved among the analyzed SARS-CoV-2 strains, except for replacement of Lysine with Arginine at 378 position of the cryptic epitope of a Shanghai isolate, hCoV-19/Shanghai/SH0007/2020 (EPI_ISL_416320). Our method of genome annotation is a promising tool for monitoring and tracking the epidemic, the associated genetic variants, and their implications for the development of effective control and prophylaxis strategy.

    Inflamm-Aging: Why Older Men Are the Most Susceptible to SARS-Cov-2 Complicated Outcomes

    Authors: Massimiliano Bonafè; Francesco Prattichizzo; Angelica Giuliani; Gianluca Storci; Jacopo Sabbatinelli; Fabiola Olivieri

    id:10.20944/preprints202004.0143.v1 Date: 2020-04-09 Source:

    Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection MESHD is characterized by a high mortality of elderly men with age-related comorbidities. In most of these patients, uncontrolled local and systemic hyperinflammation induces severe and often lethal outcomes. The aging process is characterized by the gradual development of a chronic subclinical systemic inflammation MESHD (inflamm-aging) and by acquired immune system impairment (immune senescence). Here, we advance the hypothesis that some key features of aging contribute to the disproportionate SARS-CoV-2 mortality suffered by elderly men. At least four well-recognized aging-related characteristics that are strongly expressed in older men go some way towards explaining why these patients account for the vast majority of fatalities: i. the presence of subclinical systemic inflammation MESHD without overt disease, ii. a blunted acquired immune system and type I interferon response due to the chronic inflammation MESHD; iii. the downregulation of ACE2 HGNC (SARS-CoV-2 receptor), which triggers inflammation MESHD, particularly in patients with age-related comorbid diseases such as type II diabetes MESHD; and iv. accelerated biological aging, as measured by epigenetic and senescence markers (e.g. telomere shortening) associated to the chronic inflammatory state. Though typical of the aged, especially of elderly men, it is conceivable that these features are also shared by some subsets of the younger population. The high mortality rate of SARS-CoV-2 infection MESHD suggests that clarification of the mechanisms of inflamm-aging and immune senescence can help combat not only age-related disorders but also SARS-CoV-2 infection MESHD.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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