Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

There are no SARS-CoV-2 protein terms in the subcorpus


SARS-CoV-2 Proteins
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    Excessive matrix metalloproteinase-1 HGNC and hyperactivation of endothelial cells occurred in COVID-19 MESHD patients and were associated with the severity of COVID-19 MESHD

    Authors: Fahim Syed; Wei Li; Ryan F Relich; Patrick M Russell; Shanxiang Zhang; Michelle K Zimmerman; Qigui Yu

    doi:10.1101/2021.01.19.21250115 Date: 2021-01-20 Source: medRxiv

    COVID-19 MESHD starts as a respiratory disease MESHD that can progress to pneumonia MESHD, severe acute respiratory syndrome MESHD (SARS), and multi-organ failure MESHD. Growing evidence suggests that COVID-19 MESHD is a systemic illness that primarily injures the vascular endothelium, yet the underlying mechanisms remain unknown. SARS-CoV-2 infection MESHD is believed to trigger a cytokine storm that plays a critical role in the pathogenesis of endothelialitis and vascular injury MESHD, eventually leading to respiratory and multi-organ failure MESHD in COVID-19 MESHD patients. We used a multiplex immunoassay to systematically profile and compare 65 inflammatory cytokines/chemokines/growth factors in plasma samples from 24 hospitalized (severe/critical) COVID-19 MESHD patients, 14 mild/moderate cases, and 13 healthy controls (HCs). Patients with severe/critical and mild/moderate COVID-19 MESHD had significantly higher plasma levels of 20 analytes than HCs. Surprisingly, only one cytokine ( MIF HGNC) was among these altered analytes, while the rest were chemokines and growth factors. In addition, only MMP-1 HGNC and VEGF-A HGNC were significantly elevated in hospitalized COVID-19 MESHD patients when compared to mild/moderate cases. Given that excessive MMP-1 HGNC plays a central role in tissue destruction in a wide variety of vascular diseases MESHD and that elevated VEGF-A HGNC, an EC activation marker, increases vascular permeability, we further studied MMP-1 HGNC enzymatic activity and other EC activation markers such as soluble forms of CD146 HGNC, ICAM-1 HGNC, and VCAM-1 HGNC. We found that plasma MMP-1 HGNC enzymatic activity and plasma levels of MMP-1 HGNC and EC activation markers were highly dysregulated in COVID-19 MESHD patients. Some dysregulations MESHD were associated with patients age or gender, but not with race. Our results demonstrate that COVID-19 MESHD patients have distinct inflammatory profiles that are distinguished from the cytokine storms in other human diseases. Excessive MMP-1 HGNC and hyperactivation of ECs occur in COVID-19 MESHD patients and are associated with the severity of COVID-19 MESHD.

    Identification of SARS-CoV-2-specific immune alterations in acutely ill patients

    Authors: Rose-Marie Rebillard; Marc Charabati; Camille Grasmuck; Abdelali Filali-Mouhim; Olivier Tastet; Nathalie Brassard; Audrey Daigneault; Lyne Bourbonniere; Renaud Balthazard; Ana Carmena Moratalla; Yves Carpentier Solorio; Negar Farzam-kia; Antoine Philippe Fournier; Elizabeth Gowing; Helene Jamann; Florent Lemaitre; Victoria Hannah Mamane; Karine Thai; Jean-Franois Cailhier; Nicolas Chomont; Andres Finzi; Michael Chasse; Madeleine Durand; Nathalie Arbour; Daniel E Kaufmann; Alexandre Prat; Catherine Larochelle

    doi:10.1101/2020.12.21.20248642 Date: 2020-12-22 Source: medRxiv

    Dysregulated immune profiles have been described in symptomatic SARS-CoV-2-infected MESHD patients. Whether the reported immune alterations are specific to SARS-CoV-2 infection MESHD or also triggered by other acute illnesses remains unclear. We performed flow cytometry analysis on fresh peripheral blood from a consecutive cohort of i) patients hospitalized with acute SARS-CoV-2 infection MESHD; ii) patients of comparable age/sex hospitalized for other acute disease MESHD (SARS-CoV-2 negative); and iii) healthy controls. Using both data-driven and hypothesis-driven analyses, we found several dysregulations in immune cell subsets (e.g. decreased proportion of T cells) that are similarly associated with acute SARS-CoV-2 infection MESHD and non- COVID-19 MESHD related acute illnesses. In contrast, we identified specific differences in myeloid and lymphocyte subsets that are associated with SARS-CoV-2 status (e.g. elevated proportion of ICAM-1 HGNC+ mature/activated neutrophils, ALCAM HGNC+ monocytes, and CD38 HGNC+CD8+ T cells). A subset of SARS-CoV-2-specific immune alterations correlated with disease severity, disease outcome at 30 days and mortality. Our data provides novel understanding of the immune dysregulation that are specifically associated with SARS-CoV-2 infection MESHD among acute care hospitalized patients. Our study lays the foundation for the development of specific biomarkers to stratify SARS-CoV-2+ patients at risk of unfavorable outcome and uncover novel candidate molecules to investigate from a therapeutic perspective.

    Mapping Systemic Inflammation and Antibody Responses in Multisystem Inflammatory Syndrome in Children (MIS-C)

    Authors: Conor Gruber; Roosheel Patel; Rebecca Trachman; Lauren Lepow; Fatima Amanat; Florian Krammer; Karen M. Wilson; Kenan Onel; Daniel Geanon; Kevin Tuballes; Manishkumar Patel; Konstantinos Mouskas; Nicole Simons; Vanessa Barcessat; Diane Del Valle; Samantha Udondem; Gurpawan Kang; Sandeep Gangadharan; George Ofori-Amanfo; Adeeb Rahman; Seunghee Kim-Schulze; Alexander Charney; Sacha Gnjatic; Bruce Gelb; Miriam Merad; Dusan Bogunovic

    doi:10.1101/2020.07.04.20142752 Date: 2020-07-06 Source: medRxiv

    Initially, the global outbreak of COVID-19 MESHD caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spared children from severe disease. However, after the initial wave of infections, clusters of a novel hyperinflammatory disease MESHD have been reported in regions with ongoing SARS-CoV-2 MESHD epidemics. While the characteristic clinical features are becoming clear, the pathophysiology remains unknown. Herein, we report on the immune profiles of eight Multisystem Inflammatory Syndrome MESHD in Children ( MIS HGNC-C) cases. We document that all MIS HGNC-C patients had evidence of prior SARS-CoV-2 exposure, mounting an antibody response with normal isotype-switching and neutralization capability. We further profiled the secreted immune response by high-dimensional cytokine assays, which identified elevated signatures of inflammation MESHD ( IL-18 HGNC and IL-6 HGNC), lymphocytic and myeloid chemotaxis and activation ( CCL3 HGNC, CCL4 HGNC, and CDCP1 HGNC) and mucosal immune dysregulation ( IL-17A HGNC, CCL20 HGNC, CCL28 HGNC). Mass cytometry immunophenotyping of peripheral blood revealed reductions of mDC1 and non-classical monocytes, as well as both NK- and T- lymphocytes, suggesting extravasation to affected tissues. Markers of activated myeloid function were also evident, including upregulation of ICAM1 HGNC and FcR1 in neutrophil and non-classical monocytes, well-documented markers in autoinflammation MESHD and autoimmunity that indicate enhanced antigen presentation and Fc-mediated responses. Finally, to assess the role for autoimmunity secondary to infection, we profiled the auto-antigen reactivity of MIS HGNC-C plasma, which revealed both known disease-associated autoantibodies (anti-La) and novel candidates that recognize endothelial, gastrointestinal and immune-cell antigens. All patients were treated with anti- IL6R HGNC antibody or IVIG, which led to rapid disease resolution tracking with normalization of inflammatory markers.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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