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MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (3)

NSP5 (1)

ProteinN (1)


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SARS-CoV-2 Proteins
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    Effect of COVID-19 MESHD on Lipid Profile and its Correlation with Acute Phase Reactants

    Authors: Jahanzeb Malik; Uzma Ishaq; Talha Laique; Amna Ashraf; Asmara Malik; Mommana Ali Rathore; Syed Muhammad Jawad Zaidi; Muhammad Javaid; Asad Mehmood

    doi:10.1101/2021.04.13.21255142 Date: 2021-04-14 Source: medRxiv

    Background and Objective Coronavirus disease 2019 MESHD ( COVID-19 MESHD) manifests as multiple clinical and pathological organ dysfunctions. It also disrupts metabolic profile due to the release of pro-inflammatory cytokines causing a systemic inflammation reaction MESHD. However, the development and correlation of dyslipidemia MESHD with acute phase reactants is unknown. This investigation was performed to assess the pathological alterations of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein (HDL), triglycerides, and total cholesterol levels in COVID-19 MESHD patients. Methods This was a prospective study performed on real-world patients to assess serum levels of LDL-C, HDL, TG, TC on COVID-19 MESHD patients (mild: 319; moderate: 391; critical: 357) hospitalized at our center between April 2020 through January 2021. Age- and gender-matched controls who had their lipid profiles in the same period were included as the control group. Results LDL-C, HDL, TG, and TC levels were significantly lower in COVID-19 MESHD patients when compared with the control group (P < 0.001, 0.047, 0.045, < 0.001, respectively). All parameters decreased gradually with COVID-19 MESHD disease severity (LDL-C: median (IQR), mild: 98 (91,134); moderate: 97 (81,113); critical: 68 (68,83); HDL: mild: 45 (37,50); moderate: 46 (41,50); critical: 40 (37,46); TG: mild: 186 (150,245); moderate: 156 (109,198); critical: 111 (98,154); TC: mild: 224 (212,238); moderate: 212 (203,213); critical: 154 (125,187)). LDL-C, TC, and TG were inversely correlated with acute phase reactants ( interleukin-6 HGNC ( IL-6 HGNC), Procalcitonin, C-reactive protein HGNC ( CRP HGNC), and D-dimers). Logistic regression demonstrated lipid profile, thyroid profile, and acute phase reactants as predictors of severity of COVID-19 MESHD disease. Conclusion Hypolipidemia MESHD develops in increasing frequency with severe COVID-19 MESHD disease. It inversely correlates with levels of acute-phase reactants, indicating SARS-COV-2 as the causative agent for alteration in lipid and thyroid levels.

    SARS-CoV-2 infection MESHD in the Syrian hamster model causes inflammation MESHD as well as type I interferon dysregulation MESHD in both respiratory and non-respiratory tissues including the heart and kidney

    Authors: Magen Francis; Una Goncin; Andrea Kroeker; Cynthia Swan; Robyn Ralph; Yao Lu; Athema Etzioni; Darryl Falzarano; Volker Gerdts; Steve Machtaler; Jason Kindrachuk; Alyson Ann Kelvin

    doi:10.1101/2021.04.07.438843 Date: 2021-04-08 Source: bioRxiv

    COVID-19 MESHD ( coronavirus disease 2019 MESHD) caused SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection MESHD is a disease affecting several organ systems. A model that captures all clinical symptoms of COVID-19 MESHD as well as long-haulers disease is needed. We investigated the host responses associated with infection in several major organ systems including the respiratory tract, the heart, and the kidneys after SARS-CoV-2 infection MESHD in Syrian hamsters. We found significant increases in inflammatory cytokines ( IL-6 HGNC, IL-1beta HGNC, and TNF HGNC) and type II interferons whereas type I interferons were inhibited. Examination of extrapulmonary tissue indicated inflammation MESHD in the kidney, liver, and heart which also lacked type I interferon upregulation. Histologically, the heart had evidence of mycarditis and microthrombi while the kidney had tubular inflammation MESHD. These results give insight into the multiorgan disease experienced by people with COVID-19 MESHD and possibly the prolonged disease in people with post-acute sequelae of SARS-CoV-2 (PASC).

    Predicting the severity of disease progression in COVID-19 MESHD at the individual and population level: A mathematical model

    Authors: Narendra Chirmule; Pradio Nair; Bela Desai; Ravindra Khare; Vivek R Nerurkar; Amitabh Gaur

    doi:10.1101/2021.04.01.21254804 Date: 2021-04-07 Source: medRxiv

    The impact of COVID-19 MESHD disease on health and economy has been global, and the magnitude of devastation is unparalleled in modern history. Any potential course of action to manage this complex disease requires the systematic and efficient analysis of data that can delineate the underlying pathogenesis. We have developed a mathematical model of disease progression to predict the clinical outcome, utilizing a set of causal factors known to contribute to COVID-19 MESHD pathology such as age, comorbidities, and certain viral and immunological parameters. Viral load and selected indicators of a dysfunctional MESHD immune response, such as cytokines IL-6 HGNC and IFNab; which contribute to the cytokine storm and fever MESHD, parameters of inflammation MESHD d-dimer and ferritin, aberrations in lymphocyte number, lymphopenia MESHD, and neutralizing antibodies were included for the analysis. The model provides a framework to unravel the multi-factorial complexities of the immune response manifested in SARS-CoV-2 infected MESHD individuals. Further, this model can be valuable to predict clinical outcome at an individual level and to develop strategies for allocating appropriate resources to mitigate severe cases at a population level.

    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: Preprints.org

    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.

    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.

    Targeting of the NLRP3 HGNC Inflammasome for early COVID-19 MESHD

    Authors: Carlo Marchetti; Kara Mould; Isak W. Tengesdal; William J. Janssen; Charles A. Dinarello

    doi:10.1101/2021.02.24.432734 Date: 2021-02-24 Source: bioRxiv

    Following entry and replication of Severe Acute Respiratory Syndrome-coronavirus MESHD 2 (SARS-CoV-2) into ACE2 expressing cells, the infected cells undergo lysis releasing more virus but also cell contents. In the lung, constitutive cytokines such as IL-1 HGNC are released together with other cell contents. A cascade of inflammatory cytokines ensues, including chemokines and IL-1{beta}, triggering both local as well as systemic inflammation MESHD. This cascade of inflammatory cytokines in patients with COVID-19 MESHD is termed Cytokine Release Syndrome ( CRS MESHD), and is associated with poor outcomes and death MESHD. Many studies reveal that blocking IL-1{beta HGNC} activities in COVID-19 MESHD patients reduces disease severity and deaths MESHD. Here we report highly significant circulating levels of IL-1{beta HGNC}, IL-1 Receptor antagonist HGNC, IL-6 HGNC, TNF HGNC, IL-10 HGNC and soluble urokinase plasminogen activator receptor HGNC in COVID-19 MESHD patients with mild or no symptoms. We also report that in circulating myeloid cells from the same patients, there is increased expression of the NOD-, LRR- and pyrin domain-containing 3 ( NLRP3 HGNC) early in the infection. We observed increased NLRP3 HGNC gene expression in myeloid cells correlated with IL-1{beta HGNC} gene expression and also with elevated circulating IL-1{beta HGNC} levels. We conclude that early in SARS-CoV-2 infection MESHD, NLRP3 HGNC activation takes place and initiates the CRS. Thus, NLRP3 HGNC is a target to reduce the organ damage of inflammatory cytokines of the CRS.

    Endogenous control of inflammation MESHD characterizes pregnant women with asymptomatic or paucisymptomatic SARS-CoV-2 infection MESHD

    Authors: Sara De Biasi; Domenico Lo Tartaro; Lara Gibellini; Annamaria Paolini; Andrew Quong; Carlene Petes; Geneve Awong; Samuel Douglas; Dongxia Lin; Jordan Nieto; Rebecca Borella; Lucia Fidanza; Marco Mattioli; Chiara Leone; Marianna Meschiari; Erica Franceschini; Luca Cicchetti; Tommaso Trenti; Mario Sarti; Massimo Girardis; Giovanni Guaraldi; Cristina Mussini; Fabio Facchinetti; Andrea Cossarizza

    doi:10.21203/rs.3.rs-263619/v1 Date: 2021-02-21 Source: ResearchSquare

    In 14 pregnant women who had asymptomatic or paucisymptomatic SARS-CoV-2 infection MESHD, we performed a detailed 38-parameter analysis of peripheral blood mononuclear cells by mass cytometry, studied the expression of T-cell master regular genes, investigated cell proliferation and cytokine production, and measured plasma levels of 62 cytokines. No patient showed lymphopenia MESHD or gross alterations of white blood cells. Unsupervised analyses revealed that most immune parameters were similar in patients and uninfected controls, apart from an increase in low density neutrophils in SARS-CoV-2 positive women. Also, patients did not show altered plasma levels of interleukin-6 HGNC or other main inflammatory molecules, but displayed significant increases of anti-inflammatory cytokines such as IL-1RA HGNC, IL-10 HGNC and IL-19 HGNC, and decreased levels of IL-17 HGNC, PD-L1 HGNC and D-dimer. The endogenous control of inflammation MESHD, as evidenced by plasma levels of soluble molecules, could be a strategy used during pregnancy to avoid virus-induced damages and maintain a normal immune response.

    Dysregulation of the Leukocyte Signaling Landscape during Acute COVID-19 MESHD

    Authors: Isaiah Turnbull; Anja Fuchs; Kenneth Remy; Michael Kelly; Elfaridah Frazier; Sarbani Ghosh; Shin-wen Chang; Monty Mazer; Annie Hess; Jennifer Leonard; Mark Hoofnagle; Marco Colonna; Richard Hotchkiss

    doi:10.21203/rs.3.rs-244150/v1 Date: 2021-02-15 Source: ResearchSquare

    The global COVID-19 pandemic MESHD has claimed the lives of more than 450,000 US citizens. Dysregulation of the immune system underlies the pathogenesis of COVID-19 MESHD, with inflammation MESHD mediated local tissue injury to the lung in the setting of suppressed systemic immune function. To define the molecular mechanisms of immune dysfunction MESHD in COVID-19 MESHD we utilized a systems immunology approach centered on the circulating leukocyte phosphoproteome measured by mass cytometry. COVID-19 MESHD is associated with wholesale activation of a broad set of signaling pathways across myeloid and lymphoid cell populations. STAT3 HGNC phosphorylation predominated in both monocytes and T cells and was tightly correlated with circulating IL-6 HGNC levels. High levels of STAT3 HGNC phosphorylation was associated with decreased markers of myeloid cell maturation/activation and decreased ex-vivo T cell IFN-gamma HGNC production, demonstrating that during COVID-19 MESHD dysregulated cellular activation is associated with suppression of immune effector cell function. Collectively, these data reconcile the systemic inflammatory response and functional immunosuppression induced by COVID-19 MESHD and suggest STAT3 HGNC signaling may be the central pathophysiologic mechanism driving immune dysfunction in COVID-19 MESHD.

    Compassionate use of rectal Ozone (O3) in severe COVID-19 MESHD pneumonia MESHD: a case-control study.

    Authors: Marcos Edgar Fernández-Cuadros; María Jesús Albaladejo-Florín; Sandra Alava-Rabasa; Juan Gallego-Galiana; Gerardo Fabiel Pérez-Cruz; Isabel Usandizaga-Elio; Enrique Pacios; David Torres-Garcia; Daiana Peña-Lora; Luz Casique-Bocanegra; María Jesús López-Muñoz; Javier Rodríguez-de-Cía; Olga Susana Pérez-Moro

    doi:10.21203/rs.3.rs-231696/v1 Date: 2021-02-11 Source: ResearchSquare

    Objectives: To evaluate effect of rectal Ozone in severe COVID-19 MESHD pneumonia MESHD and to compare to Standard-of-care (SOC). Material and Methods: In a case-control study, 14 patients with severe bilateral COVID-19 MESHD pneumonia MESHD (positive RT-PCR), treated with SOC and rectal Ozone, were evaluated before-and-after treatment and compared with SOC (14 patients) in a 10 day follow-up period. Ozone-protocol consisted of 8 sessions (1 session/day) of intra-rectal Ozone, (150mL volume, 35mg/ml concentration [5.25mg total dose]). The SOC-protocol included O 2- supply, antivirals (Remdesivir), corticosteroids (Dexamethasone/Metilprednisolone), monoclonal antibodies (Anakinra/Tocilizumab), antibiotics (Azytromicine), anticoagulants (Enoxaparine) and hyperimmune serum (if necessary). Primary outcome variables: a) clinical (O 2- saturation and O 2- supply); b) biochemical (Lymphocyte count, Fibrinogen HGNC, D-Dimer, Urea, Ferritin, LDH, IL-6 HGNC and CRP HGNC); c) radiological Taylor Scale. Secondary outcome variables: a) hospitalization length-of-stay, b) mortality-rate. Results: At baseline, Ozone/SOC-groups were not different on age, comorbidities, O 2 -saturation and O 2 -supply. Patients in Ozone-Group improved O 2- saturation and decrease O 2- supply. SOC maintained O 2- saturation and required more O 2- supply. Lymphocyte-count improved only in Ozone-group and with statistical difference (p<0.05). Biomarkers of inflammation MESHD ( Fibrinogen HGNC, D-Dimer, Urea, LDH, CRP HGNC and IL-6 HGNC) decreased in both groups, but only significantly in favor of Ozone-group (p<0.05). Ferritin showed a significant decrease in the Ozone-group but an increase on the SOC-Group. Radiological pneumonitis MESHD decreased on both groups but the decrease was only significant in the Ozone-Group (p<0.0001). Mortality and length-of-stay, although not significant, were inferior in Ozone-Group. Conclusion: Compassionate use of Rectal Ozone improved O 2 -saturation, reduced O 2 -supply, decreased inflammation MESHD biomarkers and improved Taylor’s radiological scale significantly when compared to SOC-Group. Mortality and length-of-stay was inferior in the Ozone-group, but this difference was not significant.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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