Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (4)

ProteinN (1)


SARS-CoV-2 Proteins
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    Clomipramine suppresses ACE2 HGNC-mediated SARS-CoV-2 entry MESHD

    Authors: Yuri Kato; Shigeru Yamada; Kazuhiro Nishiyama; Ayano Satsuka; Suyong Re; Daiki Tomokiyo; Jae Man Lee; Tomohiro Tanaka; Akiyuki Nishimura; Kenzo Yonemitsu; Hiroshi Asakura; Yuko Ibuki; Yumiko Imai; Noriho Kamiya; Kenji Mizuguchi; Takahiro Kusakabe; Yasunari Kanda; Motohiro Nishida

    doi:10.1101/2021.03.13.435221 Date: 2021-03-14 Source: bioRxiv

    Myocardial damage caused by the newly emerged coronavirus ( SARS-CoV-2) infection MESHD is one of key determinants of COVID-19 MESHD severity and mortality. SARS-CoV-2 entry to host cells are initiated by binding with its receptor, angiotensin converting enzyme (ACE) 2 HGNC, and the ACE2 HGNC abundance is thought to reflect the susceptibility to infection. Here, we found that clomipramine, a tricyclic antidepressant, potently inhibits SARS-CoV-2 infection MESHD and metabolic disorder MESHD in human iPS-derived cardiomyocytes. Among 13 approved drugs that we have previously identified as potential inhibitor of doxorubicin-induced cardiotoxicity MESHD, clomipramine showed the best potency to inhibit SARS-CoV-2 spike PROTEIN glycoprotein pseudovirus-stimulated ACE2 HGNC internalization. Indeed, SARS-CoV-2 infection MESHD to human iPS-derived cardiomyocytes (iPS-CMs) and TMPRSS2 HGNC-expressing VeroE6 cells were dramatically suppressed even after treatment with clomipramine. Furthermore, the combined use of clomipramine and remdesivir was revealed to synergistically suppress SARS-CoV-2 infection MESHD. Our results will provide the potentiality of clomipramine for the breakthrough treatment of severe COVID-19 MESHD.

    SARS-CoV-2 direct cardiac damage through spike-mediated cardiomyocyte fusion

    Authors: Jay Schneider; David Pease; Chanakha Navaratnarajah; Peter Halfmann; Daniel Clemens; Dan Ye; Changsung Kim; Alison Barkhymer; Stephen Cohle; Aron Banks; Arpit Mehta; Joseph Rantus; Tim Emmerzaal; Tamas Kozicz; Kyle Howell; Jon Charlesworth; Trace Christensen; Yoshihiro Kawaoka; Leslie Cooper; Michael Ackerman; Roberto Cattaneo

    doi:10.21203/ Date: 2020-10-20 Source: ResearchSquare

    Viruses spread between hosts through particles, but within hosts, viral genomes can spread from cell to cell through fusion, evading antiviral defenses and obviating costly infectious virion production1-3. Billions of electromechanically coupled cardiomyocytes (CMs) make myocardium inherently vulnerable to pathological electromechanical short circuits caused by intercellular viral spread 4-6. Beyond respiratory illness MESHD, COVID-19 MESHD affects the heart7 and cardiac injury and arrhythmias MESHD are serious public health concerns8-12. By studying myocardium of a young woman who died suddenly, diagnosed postmortem with COVID-19 MESHD, we discovered highly focal myocardial SARS-CoV-2 infection MESHD SARS-CoV-2 infection MESHD spreading from one CM to another through intercellular junctions identified by highly concentrated sarcolemmal t-tubule viral spike glycoprotein PROTEIN. SARS-CoV-2 permissively infected beating human induced pluripotent stem cell (hiPSC)-CMs building multinucleated cardiomyotubes (CMTs) through cell type-specific fusion driven by proteolytically-activated spike glycoprotein PROTEIN. Recombinant spike glycoprotein PROTEIN, co-localizing to sarcolemma and sarcoplasmic reticulum, produced multinucleated CMTs with pathological structure, electrophysiology and Ca2+ excitation-contraction coupling. Blocking cleavage, a peptide-based protease inhibitor neutralized SARS-CoV-2 spike PROTEIN glycoprotein pathogenicity. We conclude that SARS-CoV-2 spike PROTEIN glycoprotein, efficiently primed, activated and strategically poised during biosynthesis, can exploit the CM’s inherent membranous connectivities to drive heart damage directly, uncoupling clinically common myocardial injury MESHD from lymphocytic myocarditis MESHD, often suspected but rarely confirmed in COVID-19 MESHD.

    The Spectrum of Cardiovascular Complications in COVID-19 MESHD- 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 2019 MESHD ( COVID-19 MESHD), is a positive-stranded RNA virus with nucleocapsid. It binds to host angiotensin-converting enzyme2 HGNC (ACE2) receptor through surface glycoprotein (S PROTEIN protein). These ACE 2 HGNC receptors are attached to the cell membranes of many organs. Thus, COVID-19 MESHD does not only result in acute respiratory distress syndrome MESHD but also affects multiple organ systems, requiring a multidisciplinary approach to manage this disease. COVID-19 MESHD can damage the myocardial cells and result in fulminant myocarditis MESHD, acute cardiac injury MESHD, cardiomyopathy MESHD, heart failure MESHD, cardiogenic shock MESHD, or arrhythmia MESHD. COVID-19 MESHD 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 MESHD, and the correlation of biomarkers with the disease activity is discussed. This literature review also highlights the important treatment options and outcomes of the individual study.

    Proteome-wide analysis of differentially-expressed SARS-CoV-2 antibodies in early COVID-19 MESHD infection

    Authors: Xiaomei Zhang; Xian Wu; Dan Wang; Minya Lu; Xin Hou; Hongye Wang; Te Liang; Jiayu Dai; Hu Duan; Yingchun Xu; Yongzhe Li; Xiaobo Yu

    doi:10.1101/2020.04.14.20064535 Date: 2020-04-20 Source: medRxiv

    Rapid and accurate tests that detect IgM and IgG antibodies to SARS-CoV-2 proteins are essential in slowing the spread of COVID-19 MESHD by identifying patients who are infected with COVID-19 MESHD. Using a SARS-CoV-2 proteome microarray developed in our lab, we comprehensively profiled both IgM and IgG antibodies in forty patients with early-stage COVID-19 MESHD, influenza, or non-influenza who had similar symptoms. The results revealed that the SARS-CoV-2 N protein PROTEIN is not an ideal biomarker for COVID-19 MESHD diagnosis because of its low immunogenicity, thus tests that rely on this marker alone will have a high false negative rate. Our data further suggest that the S protein PROTEIN subunit 1 receptor binding domain (S1-RBD) might be the optimal antigen for IgM antibody detection, while the S protein PROTEIN extracellular domain (S1+S2ECD) would be the optimal antigen for both IgM and IgG antibody detection. Notably, the combination of all IgM and IgG biomarkers can identify 87% and 73.3% COVID-19 MESHD patients, respectively. Finally, the COVID-19 MESHD-specific antibodies are significantly correlated with the clinical indices of viral infection MESHD and acute myocardial injury MESHD (p[≤]0.05). Our data may help understand the function of anti-SARS-CoV-2 antibodies and improve serology tests for rapid COVID-19 MESHD screening.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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