Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (15)

ProteinN (6)

NSP5 (4)

ProteinS1 (3)

NSP3 (2)


SARS-CoV-2 Proteins
    displaying 11 - 20 records in total 439
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    Authors: Mercedes Garcia Gasalla; Juana M Ferrer; Pablo A Fraile-Ribot; Adrian Ferre-Beltran; Adrian Rodriguez; Natalia Martinez-Pomar; Luisa Ramon-Clar; Amanda Iglesias; Francisco Fanjul; Joan A Pou; Isabel LLompart; Ines Losada; Nuria Toledo; Jaime Pons; Antonio Oliver; Melchor Riera; Javier Murillas

    doi:10.1101/2021.03.17.21253816 Date: 2021-03-20 Source: medRxiv

    Introduction: Early identification of COVID-19 MESHD patients at risk of critical illness is challenging for clinicians. Immunological, virological, and routine laboratory markers to be used in addition to clinical data are needed. Aim and methods: Blood tests to measure neutrophil/lymphocyte ratio (NLR), levels of ferritin, CRP HGNC, D-dimer, complement components (C3, C4), lymphocyte subsets, and cytokines, and SARS-Cov2 RT-PCR tests were performed in COVID-19 MESHD confirmed cases within 48 hours of admission. Cycle threshold (Ct) values were determined by RT-PCR from oral or nasopharyngeal swabs on the day of admission. Severity of symptoms was categorized as mild (grade 1), severe (grade 2), and critical (grade 3). Results: 120 patients were included. COVID-19 MESHD was mild in 49, severe in 32, and critical in 39. Ferritin >370 ng/mL (OR 16.4, 95% CI 5.3-50.8), D-dimer >440 ng/mL (OR 5.45, 95% CI 2.36-12.61), CRP >7.65 mg/dL (OR 11.54, 95% CI 4.3-30.8), NLR >3.77 (OR 13.4, 95% CI 4.3-41.1), IL-6 HGNC >142.5 pg/mL (OR 8.76, 95% CI 3.56-21.54), IL-10 HGNC >10.8 pg/mL (OR 16.45, 95% CI 5.32-50.81), sIL-2r (sCD25) >804.5 pg/mL (OR 14.06, 95% CI 4.56-43.28), IL-1Ra HGNC >88.4 pg/mL (OR 4.54, 95% CI 2.03-10.17), and IL-18 HGNC >144 pg/mL (OR 17.85, 95% CI 6.54-48.78) were associated with critical COVID-19 MESHD in the univariate age-adjusted analysis. In the multivariate age-adjusted analysis, this association was confirmed only for ferritin, CRP HGNC,NLR, IL-10 HGNC, sIL-2r, and IL-18 HGNC. T, B, and NK cells were significantly decreased in critical patients. SARS-CoV-2 was undetected in blood except in 3 patients with indeterminate results. Ct values determined by RT-PCR from oral/nasopharyngeal swabs on admission were not related to symptom severity. Conclusion: levels of ferritin, D-dimer, CRP HGNC, NLR, and cytokines and cytokine receptors IL-6 HGNC, IL1-Ra HGNC, sCD25, IL-18 HGNC, and IL-10 HGNC, taken together with clinical data, can contribute to the early identification of critical COVID-19 MESHD patients.

    A proteome-wide genetic investigation identifies several SARS-CoV-2-exploited host targets of clinical relevance

    Authors: Mohd Anisul Karim; Jarrod Shilts; Jeremy Schwartzentruber; James Hayhurst; Annalisa Buniello; Elmutaz Shaikho Elhaj Mohammed; Jie Zheng; Michael V. Holmes; David Ochoa; Miguel Carmona; Joseph Maranville; Tom R. Gaunt; Valur Emilsson; Vilmundur Gudnason; Ellen M. McDonagh; Gavin J. Wright; Maya Ghoussaini; Ian Dunham

    doi:10.1101/2021.03.15.21253625 Date: 2021-03-17 Source: medRxiv

    The virus SARS-CoV-2 can exploit biological vulnerabilities in susceptible hosts that predispose to development of severe COVID-19 MESHD. Previous reports have identified several host proteins related to the interferon response (e.g. OAS1 HGNC), interleukin-6 HGNC signalling ( IL-6R HGNC), and the coagulation cascade (linked via ABO HGNC) that were associated with risk of COVID-19 MESHD. In the present study, we performed proteome-wide genetic colocalisation tests leveraging publicly available protein and COVID-19 MESHD datasets, to identify additional proteins that may contribute to COVID-19 MESHD risk. Our analytic approach identified several known targets (e.g. ABO HGNC, OAS1 HGNC), but also nominated new proteins such as soluble FAS (colocalisation probability > 0.9, p = 1 x 10-4), implicating FAS-mediated apoptosis as a potential target for COVID-19 MESHD risk. We also undertook polygenic (pan) and cis-Mendelian randomisation analyses that showed consistent associations of genetically predicted ABO HGNC protein with several COVID-19 MESHD phenotypes. The ABO HGNC signal was associated with plasma concentrations of several proteins, with the strongest association observed with CD209 HGNC in several proteomic datasets. We demonstrated experimentally that CD209 HGNC directly interacts with the spike protein PROTEIN of SARS-CoV-2, suggesting a mechanism that could explain the ABO HGNC association with COVID-19 MESHD. Our work provides a prioritised list of host targets potentially exploited by SARS-CoV-2 and is a precursor for further research on CD209 HGNC and FAS as therapeutically tractable targets for COVID-19 MESHD.

    Tocilizumab Effect in COVID-19 MESHD Hospitalized Patients: A Systematic Review and Meta-Analysis of Randomized Control Trials

    Authors: Waleed Tharwat Aletreby; Basheer Abdulrahman; Ahmed Fouad Mady; Alfateh Mohammed Noor; Mohammed H Lhmdi; Fahad Faqihi; Abdulrahman M Alharthy; Mohammed A Al-Odat; Dimitrios Karakitsos; Ziad Memish

    doi:10.1101/2021.03.15.21253581 Date: 2021-03-17 Source: medRxiv

    Since the emergence of the first cases of COVID-19 MESHD viral pneumonia MESHD late 2019 several studies evaluated the benefits of different treatment modalities. Early in the pandemic, the interleukin 6 HGNC (IL-6) receptor antibody Tocilizumab was considered in view of the cytokine release syndrome associated with COVID-19 MESHD infection. Several early observational studies showed beneficial effect of treatment with Tocilizumab on mortality, however, results from well-designed randomized clinical trials (RCT) were contradicting. ObjectivesTo perform a systematic literature review and meta-analysis of RCTs utilizing Tocilizumab in the treatment of COVID-19 MESHD pneumonia MESHD, with in-hospital mortality as a primary objective, while secondary objectives included composite outcome of mortality, intubation, or ICU admission, another secondary outcome was super added infection. MethodThis was a random effects model (DerSimonian and Laird) model of relative risk (RR), along with corresponding 95% confidence intervals, p values, and forest plots of both primary and secondary outcomes. A fixed effect sensitivity test was performed for the primary outcome, in addition to subgroup and meta-regression analyses with predefined criteria. ResultsThe primary outcome of mortality showed statistically insignificant reduction of mortality with Tocilizumab (RR = 0.9, 95% CI: 0.8 - 1.01; p = 0.09) although with an unmistakable apparent clinical benefit. There was a significant reduction in the RR of the secondary composite outcome (RR = 0.83, 95% CI: 0.76 - 0.9; p < 0.001), and no difference between groups in super-added infection (RR = 0.77, 95% CI: 0.51 - 1.19; p = 0.24). Treatment protocol allowing a second dose was the only significant predictor of improved mortality in the meta-regression analysis. Certainty of evidence was reduced to moderate for the primary outcome and the secondary outcome of clinical deterioration, while it was reduced to low for the secondary outcome of super-added infection. ConclusionModerate certainty of evidence suggest no statistically significant improvement of 28-30 day all-cause mortality of hospitalized COVID-19 MESHD patients treated with TCZ, although there may be clinically important value. Moderate certainty of evidence suggest lowered relative risk of a composite outcome of death MESHD or clinical deterioration, while, low grade evidence indicate no increase in the risk of super-added infection associated with TCZ treatment. A protocol allowing two doses of TCZ shows evidence of improved mortality as compared to a strictly single dose protocol.

    SARS-CoV-2 spike PROTEIN protein induces inflammation MESHD via TLR2 HGNC-dependent activation of the NF-κB pathway

    Authors: Shahanshah Khan; Mahnoush S. Shafiei; Christopher Longoria; John Schoggins; Rashmin C. Savani; Hasan Zaki

    doi:10.1101/2021.03.16.435700 Date: 2021-03-17 Source: bioRxiv

    Pathogenesis of COVID-19 MESHD is associated with a hyperinflammatory response; however, the precise mechanism of SARS-CoV-2-induced inflammation MESHD is poorly understood. Here we investigated direct inflammatory functions of major structural proteins of SARS-CoV-2. We observed that spike (S) protein PROTEIN potently induces inflammatory cytokines and chemokines including IL-6 HGNC, IL-1b HGNC, TNFa HGNC, CXCL1 HGNC, CXCL2 HGNC, and CCL2 HGNC, but not IFNs in human and mouse macrophages. No such inflammatory response was observed in response to membrane (M), envelope (E), and neucleocapsid ( N) proteins PROTEIN. When stimulated with extracellular S protein PROTEIN, human lung epithelial cells A549 also produce inflammatory cytokines and chemokines. Interestingly, epithelial cells expressing S protein PROTEIN intracellularly are non-inflammatory, but elicit an inflammatory response in macrophages when co-cultured. Biochemical studies revealed that S protein PROTEIN triggers inflammation MESHD via activation of the NF-kB pathway in a MyD88 HGNC-dependent manner. Further, such an activation of the NF-kB pathway is abrogated in Tlr2 HGNC-deficient macrophages. Consistently, administration of S protein PROTEIN induces IL-6, TNF-a, and IL-1b in wild-type, but not Tlr2-deficient mice. Together these data reveal a mechanism for the cytokine storm during SARS-CoV-2 infection MESHD and suggest that TLR2 could be a potential therapeutic target for 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.

    Mast Cells and COVID-19 MESHD: a case report implicating a role of mast cell activation in the prevention and treatment of Covid-19 MESHD

    Authors: Isabelle Brock; Anne Maitland

    doi:10.21203/ Date: 2021-03-15 Source: ResearchSquare

    Coronavirus disease MESHD ( COVID-19 MESHD) is a heterogeneous syndrome MESHD following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection MESHD of the upper respiratory tract. ln adults, the clinical condition can range from asymptomatic cases to severe acute respiratory syndrome MESHD and multi-organ dysfunction MESHD. Those at risk of developing COVID-19 MESHD related hyperinflammatory syndrome MESHD likely had an ineffective, innate immune response to this novel pathogen. Mast cells are associated with the epithelium, contributing to tissue homeostasis and epithelial barrier defense. Equipped with an array of pathogen receptors, mast cells exhibit distinct cytokine profiles, dependent on the tissue and the triggered pathogen receptors. Following viral infections, mast cells produce pro-inflammatory chemical mediators, such as interleukin-1 (IL-1) and IL-6 HGNC, and these cytokines has been shown to be elevated in severe COVID-19 MESHD cases. Here, we present a case of a patient with a longstanding history of signs and symptoms, worrisome for a mast cell activation syndrome MESHD ( MCAS MESHD), but never had laboratory confirmation of this non-clonal mast cell activation disorder, until she contracted COVID-19 MESHD. This case illustrates the need to recognize the rate of mast cell activation in SARS-CoV-2 infection MESHD, not only to optimize anti-SARS-CoV-2 therapy, including the development of vaccine, but to potentially curb the risk of SARS­ CoV-2 triggered hyperinflammatory syndrome MESHD.

    Single-Arm, Open-Label Phase 2 Trial of Preemptive Methylprednisolone to Avert Progression to Respiratory Failure MESHD in High-Risk Patients with COVID-19 MESHD

    Authors: Fernando Cabanillas; Javier Morales; Jose G. Conde; Jorge Bertran-Pasarell; Ricardo Fernandez; Yaimara Hernandez-Silva; Idalia Liboy; James Bryan-Diaz; Juan Arraut-Gonzalez

    doi:10.1101/2021.03.08.21253117 Date: 2021-03-09 Source: medRxiv

    Introduction: Covid-19 MESHD is a triphasic disorder first typified by a viral phase that lasts from the first onset of symptoms until seven days later. This is followed by a second and third phase, initially characterized by the appearance of lung infiltrates, followed in 20% by respiratory failure MESHD. The second phase is usually heralded by an elevation of serologic inflammatory markers including CRP HGNC, ferritin, IL-6 HGNC, LDH as well as D-dimers. Approximately 20% proceed to the second phase and are usually then treated with dexamethasone, provided they are oxygen-dependent since these are the only cases that benefit from dexamethasone. If we had objective criteria to predict this 20% that develop severe illness, they could preemptively be treated with steroids. In this exploratory study we investigated the early use of preemptive steroids in the setting of early disease, in high-risk non-oxygen dependent cases. Methods: Eligible patients were those 21 years or older with a diagnosis of Covid-19 MESHD and oxygen saturation >91%. For patients to be classified as high-risk, they had to exhibit two or more of the following abnormalities 7-10 days after first symptom: IL-6 HGNC > 10 pg/ml, ferritin > 500 ng/ml, D-dimer > 1 mg/L (1,000 ng/ml), CRP HGNC > 10 mg/dL (100 mg/L), LDH above normal range lymphopenia MESHD (absolute lymphocyte count <1,000 /microliter), oxygen saturation between 91-94%, or CT chest with evidence of ground glass infiltrates. Primary endpoint was progression to respiratory failure MESHD. CALL score method was used to predict the expected number of cases of respiratory failure MESHD. High risk patients received methylprednisolone (MPS) 80 mg IV daily x 5 days starting no earlier than seven days from first onset of symptoms. The primary endpoint was progression to hypoxemic respiratory failure MESHD defined as PaO2 <60 mm Hg or oxygen saturation <90%. Secondary endpoints included survival at 28 days from registration, admission to intensive care and live discharge from the hospital. Change in levels of inflammatory markers and length of hospitalization were also assessed. Results In 76 patients, the expected number with respiratory failure MESHD was 30 (39.5%), yet only 4 (5.3%) developed that complication (p=.00001). Survival at 28 days was 98.6%. Improvement in inflammatory markers correlated with favorable outcome. Conclusions Our results are encouraging and suggest that this approach is both effective and safe.

    Soluble angiotensin-converting enzyme 2 HGNC is transiently elevated in COVID-19 MESHD and correlates with specific inflammatory and endothelial markers

    Authors: Annika Lundstrom; Louise Ziegler; Sebastian Havervall; Ann-Sofie Rudberg; Fien Von Meijenfeldt; Ton Lisman; Nigel Mackman; Per Sanden; Charlotte Thalin

    doi:10.1101/2021.03.03.21252841 Date: 2021-03-05 Source: medRxiv

    RationaleAngiotensin-converting enzyme 2 ( ACE2 HGNC) is the main entry receptor of severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), but how SARS-CoV-2 interactions with ACE2 HGNC influences the renin-angiotensin system (RAS) in Coronavirus disease 2019 MESHD ( COVID-19 MESHD) is unknown. ObjectiveTo measure circulating ACE2 HGNC and ACE HGNC levels in COVID-19 MESHD patients and investigate association with risk factors, outcome and inflammatory markers. Methods and resultsSoluble ACE2 HGNC (sACE2) and sACE concentrations were measured by ELISA in plasma samples from 114 hospital-treated COVID-19 MESHD patients and 10 healthy controls. Follow-up samples after four months were available for 58/114 patients. Von Willebrand MESHD Von Willebrand HGNC factor ( VWF HGNC), factor VIII ( fVIII HGNC), D-dimer, interleukin 6 ( IL-6 HGNC), tumor necrosis MESHD factor and plasminogen activator inhibitor 1 ( PAI-1 HGNC) had previously been determined. Levels of sACE2 were higher in COVID-19 MESHD patients than in healthy controls, median 5.0 (interquartile range 2.8-11.8) ng/ml versus 1.4 (1.1-1.6) ng/ml, p < 0.0001. sACE2 was higher in men than women, but were not affected by other risk factors for severe COVID-19 MESHD. sACE 2 decreased to 2.3 (1.6-3.9) ng/ml at follow-up, p < 0.0001, but remained higher than in healthy controls, p=0.012. Follow-up sACE2 levels were higher with increasing age, BMI, total number of comorbidities, for patients with diabetes MESHD and patients on RAS-inhibition. sACE was marginally lower during COVID-19 MESHD compared with at follow-up, 57 (45-70) ng/ml versus 72 (52-87) ng/ml, p=0.008. Levels of sACE2 and sACE did not differ depending on survival or disease severity (care level, respiratory support). sACE2 during COVID-19 MESHD correlated with VWF HGNC, fVIII HGNC and D-dimer, while sACE correlated with IL-6 HGNC, TNF HGNC and PAI-1 HGNC. ConclusionssACE2 was transiently elevated in COVID-19 MESHD, likely due to increased shedding from infected cells. sACE2 and sACE during COVID-19 MESHD differed distinctly in their correlations with markers of inflammation MESHD and endothelial dysfunction, suggesting release from different cell types and/or vascular beds.

    Clinical course and risk factors for in-hospital mortality of 205 patients with SARS-CoV-2 pneumonia MESHD in Como, Lombardy Region, Italy

    Authors: Mauro Turrini; Angelo Gardellini; Livia Beretta; Lucia Buzzi; Stefano Ferrario; Sabrina Vasile; Raffaella Clerici; Andrea Colzani; Luigi Liparulo; Giovanni Scognamiglio; Gianni Imperiali; Giovanni Corrado; Antonella Strada; Marco Galletti; Nunzio Castiglione; Claudio Zanon

    doi:10.1101/2021.02.25.20134866 Date: 2021-03-05 Source: medRxiv

    Importance: With randomized clinical trials ongoing and vaccine still a long distance away, efforts to repurpose old medications used for other diseases provide hope for treatment of COVID-19 MESHD. Objectives: To examine the risk factors for in-hospital mortality and describe the effectiveness of different treatment strategies in a real-life setting of patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia MESHD. Design: Real-life single-center study during the Lombardy COVID-19 MESHD outbreak. Setting: Valduce Hospital in Como, Lombardy Region, Italy. Participants: 205 laboratory-confirmed patients presenting with SARS-Cov-2 pneumonia MESHD requiring hospitalization. Interventions: All patients received best supportive care and, based on their clinical needs and comorbidities, specific interventions that included the main drugs being tested for repurposing to treat COVID-19 MESHD, such as hydroxychloroquine, anticoagulation, antiviral drugs, steroids or interleukin-6 HGNC pathway inhibitors. Main outcomes and measures: Clinical, laboratory and treatment characteristics were analyzed with univariate and multivariate logistic regression methods to explore their impact on in-hospital mortality and compared with current literature data. Results: Univariate analyses for clinical variables showed prognostic significance for age equal or greater than 70 years (estimated 28-days survival: 21.4 vs 67.4%; p<0.0001), presence of 2 or more relevant comorbidities (35.3 vs 61.8%; p=0.0008), ratio of arterial oxygen partial pressure to fractional inspired oxygen (P/F) less than 200 at presentation (21-days survival: 14.7 vs 52.4%;p<0.0001), high levels of lactate dehydrogenase (LDH) (26.4 vs 65.3%; p=0.0001), and elevated C-reactive protein HGNC (CRP) values (25.4 vs 74.9%; p=0.0001), while no statistical significance was found for all the other clinical variables tested. At univariate analysis for the different treatment scheduled, prognostic significance for survival was showed for intermediate or therapeutic-dose anticoagulation (estimated 28-days survival: 37.1 vs 23.4%; p=0.0001), hydroxychloroquine (35.7 vs 27.3%; p=0.0029), early antiviral therapy with lopinavir/ritonavir (60.1 vs 22.4%; p<0.0001), late short-course of steroids (47.9 vs 18.2%; p<0.0001) or tocilizumab therapy (69.4 vs 29.4%; p=0.0059). Multivariable regression confirmed increasing odds of in-hospital death associated with age older than 70 years (odds ratio 3.26, 95% CI 1.81 - 5.86; p<0.0001) and showed a reduction in mortality for patients treated with anticoagulant (-0.37, 0.49 - 0.95; p=0.0273), antiviral (-1.22, 0.16 - 0.54; p<0.0001), or steroids (-0.59, 0.35 - 0.87; p=0.0117) therapy.

    Ribosome-profiling reveals restricted post transcriptional ex-pression of antiviral cytokines and transcription factors during SARS-CoV-2 infection MESHD

    Authors: Marina R Alexander; Aaron M Brice; Petrus Jansen Van Vuren; Christina Rootes; Leon Tribolet; Christopher Cowled; Andrew G.D. Bean; Cameron R Stewart

    doi:10.1101/2021.03.03.433675 Date: 2021-03-04 Source: bioRxiv

    The global COVID-19 pandemic MESHD caused by SARS-CoV-2 has resulted in over 2.2 million deaths. Disease outcomes range from asymptomatic to severe with, so far, minimal genotypic change to the virus so understanding the host response is paramount. Transcriptomics has become incredibly important in understanding host-pathogen interactions; however, post-transcriptional regulation plays an important role in infection and immunity through translation and mRNA stability, al-lowing tight control over potent host responses by both the host and the invading virus. Here we apply ribosome profiling to assess post-transcriptional regulation of host genes during SARS-CoV-2 infection MESHD of a human lung epithelial cell line (Calu-3). We have identified numerous transcription factors ( JUN HGNC, ZBTB20 HGNC, ATF3 HGNC, HIVEP2 HGNC and EGR1 HGNC) as well as select antiviral cytokine genes, namely IFNB1 HGNC, IFNL1,2 and 3, IL-6 HGNC and CCL5 HGNC, that are restricted at the post-transcriptional level by SARS-CoV-2 infection MESHD and discuss the impact this would have on the host response to infection. This early phase restriction of antiviral transcripts in the lungs may allow high viral load and consequent immune dysregulation typically seen in SARS-CoV-2 infection MESHD.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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