Corpus overview


MeSH Disease

Human Phenotype


    displaying 1 - 10 records in total 1316
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    Prediction and Analysis of SARS-CoV-2-Targeting microRNA in Human Lung Epithelium

    Authors: Jonathan Tak-Sum Chow; Leonardo Salmena

    id:10.20944/preprints202008.0253.v1 Date: 2020-08-11 Source:

    Severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2), an RNA virus, is responsible for coronavirus disease MESHD 2019 (COVID-19) pandemic of 2020. Experimental evidence suggests that microRNA can mediate an intracellular defence mechanism against some RNA viruses. The purpose of this study was to identify microRNA with predicted binding sites in the SARS-CoV-2 genome, compare these to their microRNA expression profiles in lung epithelial tissue and make inference towards possible roles for microRNA in mitigating coronavirus infection MESHD. We hypothesize that high expression of specific coronavirus-targeting microRNA in lung epithelia may protect against infection MESHD and viral propagation, conversely low expression may confer susceptibility to infection MESHD. We have identified 128 human microRNA with potential to target the SARS-CoV-2 genome, most of which have very low expression in lung epithelia. Six of these 128 microRNA are differentially expressed upon in vitro infection MESHD of SARS-CoV-2. Twenty-eight and 23 microRNA also target the SARS-CoV and MERS-CoV, respectively. In addition, 48 and 32 microRNA are commonly identified in two other studies. Further research into identifying bona fide coronavirus targeting microRNA will be useful in understanding the importance of microRNA as cellular defence mechanism against pathogenic coronavirus infections MESHD.

    The Spectrum of Cardiovascular Complications in COVID-19- A Comprehensive Literature Review

    Authors: Raja Shakeel Mushtaque; Rabia Mushtaque; Shahbano Baloch; Aadil Raza; Haseeb Bhatti; Zohaib Khan

    id:10.20944/preprints202008.0257.v1 Date: 2020-08-11 Source:

    A newly identified novel coronavirus named as severe acute respiratory syndrome MESHD-related coronavirus2 (SARS‐CoV 2) has given rise to the global pandemic. SARS-CoV2 which causes coronavirus disease MESHD 2019 (COVID-19), is a positive-stranded RNA virus with nucleocapsid. It binds to host angiotensin-converting enzyme2 (ACE2) receptor through surface glycoprotein (S protein). These ACE 2 receptors are attached to the cell membranes of many organs. Thus, COVID-19 does not only result in acute respiratory distress HP syndrome MESHD but also affects multiple organ systems, requiring a multidisciplinary approach to manage this disease MESHD. COVID-19 can damage the myocardial cells and result in fulminant myocarditis MESHD myocarditis HP, acute cardiac injury, cardiomyopathy MESHD cardiomyopathy HP, heart failure MESHD, cardiogenic shock MESHD cardiogenic shock HP, or arrhythmia HP. COVID-19 seeds harmful immune response through cytokine storm leading to indirect organ damage. In this literature review, the available data is comprehended regarding cardiovascular complications in COVID-19, and the correlation of biomarkers with the disease MESHD activity is discussed. This literature review also highlights the important treatment options and outcomes of the individual study.

    Petabase-scale sequence alignment catalyses viral discovery

    Authors: Robert C Edgar; Jeff Taylor; Tomer Altman; Pierre Barbera; Dmitry Meleshko; Victor Lin; Dan Lohr; Gherman Novakovsky; Basem Al-Shayeb; Jill Banfield; Anton Korobeynikov; Rayan Chikhi; Artem Babaian

    doi:10.1101/2020.08.07.241729 Date: 2020-08-10 Source: bioRxiv

    Public sequence data represents a major opportunity for viral discovery, but its exploration has been inhibited by a lack of efficient methods for searching this corpus, which is currently at the petabase scale and growing exponentially. To address the ongoing pandemic caused by Severe Acute Respiratory Syndrome MESHD Coronavirus 2 and expand the known sequence diversity of viruses, we aligned pangenomes for coronaviruses (CoV) and other viral families to 5.6 petabases of public sequencing data from 3.8 million biologically diverse samples. To implement this strategy, we developed a cloud computing architecture, `Serratus`, tailored for ultra-high throughput sequence alignment at the petabase scale. From this search, we identified and assembled thousands of CoV and CoV-like genomes and genome fragments ranging from known strains to putatively novel genera. We generalise this strategy to other viral families, identifying several novel deltaviruses and huge bacteriophages. To catalyse a new era of viral discovery we made millions of viral alignments and family identifications freely available to the research community ( Expanding the known diversity and zoonotic reservoirs of CoV and other emerging pathogens can accelerate vaccine and therapeutic developments for the current pandemic, and help us anticipate and mitigate future ones.

    Potential Phytopharmaceutical Constituents of Solanum Trilobatum L. as Significant Inhibitors Against COVID-19: Robust-Binding Mode of Inhibition by Molecular Docking, PASS-Aid Bioactivity and ADMET Investigations

    Authors: Shanmugam Anandakumar; Damodharan Kannan; Eugene Wilson; Kasthuri Bai Narayanan; Ganesan Suresh; Kadarkarai Kanakavalli; Muthu Tamizh Manoharan

    doi:10.26434/chemrxiv.12781754.v1 Date: 2020-08-10 Source: ChemRxiv

    The novel coronavirus is better known as COVID–19 caused by Severe Acute Respiratory Syndrome MESHD Corona–Virus 2 (SARS–CoV–2) which initially outburst at Wuhan in China on December 2019 and spread very rapidly around the globe. Scientists from the global regions endeavours to still probe for detecting potential treatment and discover effective therapeutic drug candidates for this unabated pandemic. In our article, we reported the molecular docking, bioactivity score, ADME and toxicity prediction of the phytoconstituents of Solanum trilobatum Linn. such as Solanidine, Solasodine and a–Solanine as potential inhibitors against the main protease (Mpro) of SARS–CoV–2 tropism. The molecular docking of Solanidine, Solasodine and a–Solanine has revealed that it bounded deep into the active cavity site on the Mpro. Further, the pharmacodynamics and bioactivity profile has confirmed that the molecules obeyed the Lipinski’s rule and will be used as notably treasured lead drug candidates to pursue further biochemical and cell–based assays to explore its potential against COVID–19 pandemic. Thus, envisioning thought–provoking research certainly provide new leads for the global researchers.

    A single-cell mathematical model of SARS-CoV-2 induced pyroptosis and the anti-inflammatory response to the drug tranilast

    Authors: Sara J Hamis; Fiona R Macfarlane

    id:2008.04172v1 Date: 2020-08-10 Source: arXiv

    Pyroptosis is an inflammatory mode of cell death MESHD that contributes to the cytokine storm associated with severe cases of coronavirus disease MESHD 2019 (COVID-19). Central to pyroptosis induced by severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2) is the formation of the NLRP3 inflammasome. Inflammasome formation, and by extension pyroptosis, may be inhibited by certain anti-inflammatory drugs. One such drug, tranilast, is currently being evaluated as a COVID-19 treatment target in a clinical trial. In this study, we present a single-cell mathematical model that captures the formation of the NLRP3 inflammasome, pyroptotic cell death MESHD and drug-responses to tranilast. The model is formulated in terms of a system of ordinary differential equations (ODEs) that describe the dynamics of proteins involved in pyroptosis. The model demonstrates that tranilast delays the formation of the NLRP3 inflammasome, and thus may alter the mode of cell death MESHD from inflammatory (pyroptosis) to non-inflammatory (e.g., apoptosis).

    mRNA induced expression of human angiotensin-converting enzyme 2 in mice for the study of the adaptive immune response to severe acute respiratory syndrome MESHD coronavirus 2

    Authors: Mariah Hassert; Elizabeth Geerling; E. Taylor Stone; Tara L. Steffen; Alexandria Dickson; Madi S. Feldman; Jacob Class; Justin M. Richner; James D Brien; Amelia K Pinto

    doi:10.1101/2020.08.07.241877 Date: 2020-08-07 Source: bioRxiv

    The novel human coronavirus, severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2) has caused a pandemic resulting in nearly 20 million infections across MESHD the globe, as of August 2020. Critical to the rapid evaluation of vaccines and antivirals is the development of tractable animal models of infection MESHD. The use of common laboratory strains of mice to this end is hindered by significant divergence of the angiotensin-converting enzyme 2 (ACE2), which is the receptor required for entry of SARS-CoV-2. In the current study, we designed and utilized an mRNA-based transfection system to induce expression of the hACE2 receptor in order to confer entry of SARS-CoV-2 in otherwise non-permissive cells. By employing this expression system in an in vivo setting, we were able to interrogate the adaptive immune response to SARS-CoV-2 in type 1 interferon receptor deficient mice. In doing so, we showed that the T cell response to SARS-CoV-2 is enhanced when hACE2 is expressed during infection MESHD. Moreover, we demonstrated that these responses are preserved in memory and are boosted upon secondary infection MESHD. Interestingly, we did not observe an enhancement of SARS-CoV-2 specific antibody SERO responses with hACE2 induction. Importantly, using this system, we functionally identified the CD4+ and CD8+ peptide epitopes targeted during SARS-CoV-2 infection MESHD in H2b restricted mice. Antigen-specific CD8+ T cells in mice of this MHC haplotype primarily target peptides of the spike and membrane proteins, while the antigen-specific CD4+ T cells target peptides of the nucleocapsid, membrane, and spike proteins. The functional identification of these T cell epitopes will be critical for evaluation of vaccine efficacy in murine models of SARS-CoV-2. The use of this tractable expression system has the potential to be used in other instances of emerging infections MESHD in which the rapid development of an animal model is hindered by a lack of host susceptibility factors.

    Generation of tonsil organoids as an ex vivo model for SARS-CoV-2 infection MESHD

    Authors: Han Kyung Kim; Hyeryeon Kim; Myoung Kyu Lee; Woo Hee Choi; Yejin Jang; Jin Soo Shin; Jun-Yeol Park; Kang Hyun Kim; Hyun Wook Han; Meehyein Kim; Young Chang Lim; Jongman Yoo

    doi:10.1101/2020.08.06.239574 Date: 2020-08-07 Source: bioRxiv

    Palatine tonsil plays role in the immune system's first line of defense against foreign pathogens. Coronavirus disease MESHD 2019 (COVID-19), caused by severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2), has become a worldwide pandemic since the infection MESHD was first reported in China in December 2019. The aim of this study was to establish tonsil epithelial cell-derived organoids and to examine their feasibility as an ex vivo model for SARS-CoV-2 infection MESHD. Using an optimized protocol, we achieved 3D tonsil organoid culture from human tonsil tissue that reflects the distinctive characteristics of the tonsil epithelium, such as its cellular composition, histologic properties, and molecular biological features. Notably, we verified that SARS-CoV-2 can infect tonsil organoids with a robust replication efficiency. Furthermore, treatment with remdesivir, an antiviral agent, effectively protected them from viral infection MESHD. Therefore, tonsil organoids could be available for investigation of SARS-CoV-2 infection MESHD-mediated pathology and for preclinical screening of novel antiviral drug candidates.

    Specificity and Performance SERO of Nucleocapsid and Spike-based SARS-CoV-2 Serologic Assays

    Authors: Zahra Rikhtegaran Tehrani; Saman Saadat; Ebtehal Saleh; Xin Ouyang; Niel Constantine; Anthony L. DeVico; Anthony D. Harris; George K. Lewis; Shyam Kottilil; Mohammad M. Sajadi

    doi:10.1101/2020.08.05.20168476 Date: 2020-08-07 Source: medRxiv

    There is an urgent need for an accurate antibody test SERO for severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2). In this paper, we have developed 3 ELISA SERO methods, trimer spike IgA, trimer spike IgG, and nucleocapsid IgG, for detecting anti- SARS-CoV-2 antibodies SERO. We evaluated their performance SERO in comparison with four commercial ELISAs SERO, EDI Novel Coronavirus COVID-19 ELISA IgG SERO and IgM, Euroimmun Anti-SARS-CoV-2 ELISA IgG SERO and IgA, and one lateral flow assay, DPP COVID-19 IgM/IgG System (Chembio). Both sensitivity SERO and specificity were evaluated and the causes of false-positive reactions were determined. The assays were compared using 300 pre-epidemic samples and 100 PCR-confirmed COVID-19 samples. The sensitivities SERO and specificities of the assays were as follows: 90%/100% (in-house trimer spike IgA), 90%/99.3% (in-house trimer spike IgG), 89%/98.3% (in-house nucleocapsid IgG), 73.7%/100% (EDI nucleocapsid IgM), 84.5%/95.1% (EDI nucleocapsid IgG), 95%/93.7% (Euroimmun S1 IgA), 82.8%/99.7% (Euroimmun S1 IgG), 82.0%/91.7% (Chembio nucleocapsid IgM), 92%/93.3% (Chembio nucleocapsid IgG). The presumed causes of positive signals from pre-epidemic samples in commercial and in-house assays were mixed. In some cases, positivity varied with assay repetition. In other cases, reactivity was abrogated by competitive inhibition (spiking the sample with analyte prior to performing the assay). In other cases, reactivity was consistently detected but not abrogated by analyte spiking. Overall, there was wide variability in assay performance SERO using our samples, with in-house tests exhibiting the highest combined sensitivity SERO and specificity. The causes of false positivity in pre-epidemic samples may be due to plasma SERO antibodies SERO apparently reacting with the analyte, or spurious reactivity may be directed against non-specific components in the assay system. Identification of these targets will be essential to improving assay performance SERO.

    Association of mental disorders with SARS-CoV-2 infection MESHD infection and severe HP and severe health outcomes: a nationwide cohort study

    Authors: Ha-Lim Jeon; Jun Soo Kwon; So-Hee Park; Ju-Young Shin

    doi:10.1101/2020.08.05.20169201 Date: 2020-08-07 Source: medRxiv

    Background: No epidemiological data exists for the association between mental disorders and the risk of severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2) infection MESHD and coronavirus disease MESHD 2019 (COVID-19) severity. Aims: To evaluate the association between mental disorders and the risk of SARS-CoV-2 infection MESHD infection and severe HP and severe outcomes following COVID-19. Methods: We performed a cohort study using the Korean COVID-19 patient database based on the national health insurance data. Each patient with a mental or behavioral disorder (diagnosed during six months prior to the first SARS-CoV-2 test) was matched by age TRANS, sex, and Charlson comorbidity index with up to four patients without mental disorders. SARS-CoV-2 positivity risk and risk of death MESHD or severe events (intensive care unit admission, use of mechanical ventilation, and acute respiratory distress HP syndrome MESHD) post- infection MESHD were calculated using conditional logistic regression analysis. Results: Among 230,565 patients tested for SARS-CoV-2, 33,653 (14.6%) had mental disorders, 928/33,653 (2.76%) tested positive, and 56/928 (6.03%) died. In multivariate analysis with the matched cohort, there was no association between mental disorders and SARS-CoV-2 positivity risk (odds ratio [OR], 1.02; 95% confidence interval [CI], 0.92-1.12); however, a higher risk was associated with schizophrenia HP-related disorders (OR, 1.36; 95% CI, 1.02-1.81). Among confirmed cases TRANS, mortality risk significantly increased in patients with mental disorders (OR, 1.84, 95% CI, 1.07-3.15). Conclusion: Mental disorders are likely contributing factors of mortality following COVID-19. Although the infection MESHD infection risk TRANS infection risk TRANS risk did not increase in overall mental disorders, patients with schizophrenia HP-related disorders were more vulnerable to the infection MESHD.

    Quickly And Simply Detection For Coronavirus Including SARS-CoV-2 On The Mobile Real-Time PCR Device And Without RNA Extraction

    Authors: Masaaki Muraoka; Yukiko Tanoi; Tetsutaro Tada; MIkio Mizukoshi; Osamu Kawaguchi

    doi:10.1101/2020.08.06.20168294 Date: 2020-08-07 Source: medRxiv

    Severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2) was reported to WHO as an outbreak in Wuhan City, Hubei Province, China on end of 2019, afterwards epidemic in many countries, and pandemic on the worldwide in 2020. Usually detection of coronavirus including SARS-CoV-2 was detected by real-time RT-PCR method, but it must be long time that RNA is treated by extraction, concentration and purification, and detected by RT-PCR method. We modified various methods, of which evaluated if each method is short and simple enough. In one point of the evaluations, real-time RT-PCR could be finished in very short time with using mobile real-time PCR device PCR1100 (Nippon Sheet Glass Co. Ltd.). It was able to detect positive control RNA for 20 minutes by each method according to the National Institute of Infections MESHD Disease MESHD in Japan (NIID), and less than 13.5 minutes according to the Centers for Disease MESHD Control and Prevention in USA (CDC). In another point of the evaluations, surprisingly, Human coronavirus 229E, which was substituted for SARS-CoV-2, could be detected in crude state without treatment in advance of RNA. As that was, it was possible to detect coronavirus with direct RT-PCR. Therefore, it might eliminate wasteful time, avoid secondary infection MESHD infection and risk TRANS infection and risk TRANS and risk of contamination. In light of the above two points, SARS-CoV-2 might be detected more quickly and more simply. With using this mobile real-time PCR, these methods should be suitable for not only SARS-CoV-2 but also other various viruses and might save time compared to earlier detection methods.

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MeSH Disease
Human Phenotype

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