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HGNC Genes

SARS-CoV-2 proteins

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SARS-CoV-2 Proteins
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    Exosomes from COVID-19 MESHD patients carry tenascin-C HGNC and fibrinogen-β in triggering inflammatory signals in distant organ cells

    Authors: Subhayan Sur; Mousumi B. Khatun; Robert Steele; Scott Isbell; Ranjit Ray; Ratna B Ray

    doi:10.1101/2021.02.08.430369 Date: 2021-02-09 Source: bioRxiv

    SARS-CoV-2 infection MESHD causes cytokine storm and overshoot immunity in humans; however, it remains to be determined whether genetic material of SARS-CoV-2 and/or virus induced soluble mediators from lung epithelial cells as natural host are carried out by macrophages or other vehicles at distant organs causing tissue damage. We speculated that exosomes as extracellular vesicles are secreted from SARS-CoV-2 infected MESHD cells may transport messages to other cells of distant organs leading to pathogenic consequences. For this, we took an unbiased proteomic approach for analyses of exosomes isolated from plasma of healthy volunteers and SARS-CoV-2 infected MESHD patients. Our results revealed that tenascin-C HGNC ( TNC HGNC) and fibrinogen-{beta} ( FGB HGNC) are highly abundant in exosomes from SARS-CoV-2 infected MESHD patient's plasma as compared to that of healthy normal controls. Since TNC HGNC and FGB HGNC stimulate pro-inflammatory cytokines via NF-kB pathway, we examined the status of TNF-a HGNC, IL-6 HGNC and CCL5 HGNC expression upon exposure of hepatocytes to exosomes from COVID-19 MESHD patients and observed significant increase when compared with that from healthy subjects. Together, our results demonstrated that soluble mediators, like TNC HGNC and FGB HGNC, are transported through plasma exosomes in SARS-CoV-2 infected MESHD patients and trigger pro-inflammatory cytokine expression in cells of distant organs in COVID-19 MESHD patients.

    CSF of SARS-CoV-2 patients with neurological syndromes reveals hints to understand pathophysiology

    Authors: Raphael Bernard-Valnet; Sylvain Perriot; Mathieu Canales; Beatrice Pizzarotti; Leonardo Caranzano; Mayte Castro-Jimenez; Jean-Benoit Epiney; Sergiu Vijiala; Paolo Salvioni Chiabotti; Angelica Anichini; Alexander Salerno; Katia Jaton; Julien Vaucher; Matthieu Perreau; Gilbert Greub; Giuseppe Pantaleo; Renaud Du Pasquier

    doi:10.1101/2020.11.01.20217497 Date: 2020-11-04 Source: medRxiv

    Objective: Coronavirus disease ( COVID-19 MESHD) has been associated with a large variety of neurological disorders MESHD. However the mechanisms underlying these neurological complications remain elusive. In this study we aimed at determining whether neurological symptoms were caused by SARS-CoV-2 direct infection of by pro-inflammatory mediators. Methods: We checked for SARS-CoV-2 RNA by RT-qPCR, SARS-CoV-2-specific antibodies and for 48 cytokines/chemokines/growth factors (by Luminex) in the cerebrospinal fluids (CSF) +/- sera of a cohort of 17 COVID-19 MESHD patients with neurological presentation and 55 neurological control patients (inflammatory [IND], non inflammatory [NIND], multiple sclerosis MESHD [ MS MESHD]). Results: We found SARS-CoV-2 RNA and antibodies specific for this virus in the CSF of 0/17 and 8/16 COVID-19 MESHD patients, respectively. The presence of SARS-CoV-2 antibodies was explained by a rupture of the blood brain barrier (passive transfer) in 6/16 (38%). An intrathecal synthesis of SARS-CoV2-specific antibodies was present in 2/16 patients. Of the four categories of tested patients, the CSF of IND exhibited the highest level of chemokines ( CCL4 HGNC, CCL5 HGNC, CXCL8 HGNC, CXCL10 HGNC, CXCL12 HGNC, and CXCL13 HGNC), followed by the CSF of MS MESHD patients ( CXCL12 HGNC, and CXCL13 HGNC). There was no significant difference between COVID-19 MESHD and NIND patients, even if some chemokines ( CCL4 HGNC, CCL5 HGNC, CXCL8 HGNC, andCXCL10) tended to be higher in the former. Interestingly, among COVD-19 patients, the CSF of those with a severe disease ( encephalitis MESHD/ encephalopathy MESHD) contained higher levels CXCL8 HGNC and CXCL10 HGNC than those with other neurological presentations. Interpretation: Our results do not show obvious SARS-CoV-2 infection MESHD SARS-CoV-2 infection MESHD of the central nervous system, but point to a mild inflammatory reaction reflecting an astrocytic reaction. Methods: We checked for SARS-CoV-2 mRNA by qPCR, SARS-CoV-2-specific antibodies and for 49 cytokines/chemokines/growth factors (by Luminex) in the cerebrospinal fluid (CSF) +/- serum of a cohort of 17 COVID-19 MESHD patients with neurological presentation and 55 neurological controls (inflammatory, non inflammatory, multiple sclerosis MESHD). Results: We found SARS-CoV-2 mRNA and antibodies specific for this virus in the CSF of 0/17 and 8/16 COVID-19 MESHD patients, respectively. The presence of SARS-CoV-2 antibodies was explained by a rupture of the blood brain barrier (passive transfer) in 6/16 (37,5%), but an intrathecal synthesis of SARS-CoV2-specific antibodies was present in 2/17.As compared to SARS-CoV-2-negative NIND patients, the CSF of IND patients exhibited the highest level of chemokines ( CCL4 HGNC, CCL5 HGNC, CXCL8 HGNC, CXCL10 HGNC, CXCL12 HGNC, and CXCL13 HGNC), followed the CSF of MS MESHD patients ( CXCL12 HGNC, and CXCL13 HGNC). There was no difference between COVID-19 MESHD patients with neurological diseases MESHD compared to NIND even if some chemokines ( CCL4 HGNC, CCL5 HGNC, CXCL8 HGNC, andCXCL10) tended to be higher than NIND. Interestingly, among COVD-19 patients, the CSF of those with a severe disease ( encephalitis MESHD/ encephalopathy MESHD) contained higher levels CXCL8 HGNC and CXCL10 HGNC than those with other neurological presentations. Interpretation: Our results confirm the absence of obvious SARS-CoV-2 infection MESHD SARS-CoV-2 infection MESHD of the central nervous system and point to a mild inflammatory reaction reflecting an astrocytic reaction.

    Disruption of the CCL5 HGNC/ RANTES HGNC- CCR5 HGNC Pathway Restores Immune Homeostasis and Reduces Plasma Viral Load in Critical COVID-19 MESHD

    Authors: Bruce K Patterson; Harish Seethamraju; Kush Dhody; Michael J Corley; Kazemm Kazempour; Jay P Lalezari; Alina PS Pang; Christopher Sugai; Edgar B Francisco; Amruta Pise; Hallison Rodrigues; Matthew Ryou; Helen L Wu; Gabriela M Webb; Byung S Park; Scott Kelly; Nadar Pourhassan; Alena Lelic; Lama Kdouh; Monica Herrera; Eric Hall; Enver Aklin; Lishomwa Ndhlovu; Jonah B Sacha

    doi:10.1101/2020.05.02.20084673 Date: 2020-05-05 Source: medRxiv

    Severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), the causative agent of coronavirus disease 2019 MESHD ( COVID-19 MESHD), is now pandemic with nearly three million cases reported to date. Although the majority of COVID-19 MESHD patients experience only mild or moderate symptoms, a subset will progress to severe disease with pneumonia MESHD and acute respiratory distress syndrome MESHD ( ARDS MESHD) requiring mechanical ventilation. Emerging results indicate a dysregulated MESHD immune response characterized by runaway inflammation MESHD, including cytokine release syndrome (CRS), as the major driver of pathology in severe COVID-19 MESHD. With no treatments currently approved for COVID-19 MESHD, therapeutics to prevent or treat the excessive inflammation MESHD in severe disease caused by SARS-CoV-2 infection MESHD are urgently needed. Here, in 10 terminally-ill, critical COVID-19 MESHD patients we report profound elevation of plasma IL-6 HGNC and CCL5 HGNC ( RANTES HGNC), decreased CD8 HGNC+ T cell levels, and SARS-CoV-2 plasma viremia MESHD. Following compassionate care treatment with the CCR5 HGNC blocking antibody leronlimab, we observed complete CCR5 HGNC receptor occupancy on macrophage and T cells, rapid reduction of plasma IL-6 HGNC, restoration of the CD4 HGNC/ CD8 HGNC ratio, and a significant decrease in SARS-CoV-2 plasma viremia MESHD. Consistent with reduction of plasma IL-6 HGNC, single-cell RNA-sequencing revealed declines MESHD in transcriptomic myeloid cell clusters expressing IL-6 HGNC and interferon-related genes. These results demonstrate a novel approach to resolving unchecked inflammation MESHD, restoring immunologic deficiencies MESHD, and reducing SARS-CoV-2 plasma viral load via disruption of the CCL5 HGNC- CCR5 HGNC axis, and support randomized clinical trials to assess clinical efficacy of leronlimab-mediated inhibition of CCR5 HGNC for COVID-19 MESHD.

    Disruption of the CCL5 HGNC/ RANTES HGNC- CCR5 HGNC Pathway Restores Immune Homeostasis and Reduces Plasma Viral Load in Critical COVID-19 MESHD

    Authors: Bruce Pattterson; Harish Seetthamraju; Kush Dhody; Michael Corley; Kazem Kazempour; Jay Lalezari; Alina Pang; Christopher Sugai; Edgar Francisco; Amruta Pise; Hallison Rodrigues; Matthew Ryou; Helen Wu; Gabriela Webb; Byung Park; Scott Kelly; Nader Pourhassan; Alena Lelic; Lama Kdouh; Monica Herrera; Eric Hall; Enver Aklin; Lishomwa Ndhlovu; Jonah Sacha

    doi:10.21203/rs.3.rs-26517/v1 Date: 2020-05-02 Source: ResearchSquare

    Severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), the causative agent of coronavirus disease 2019 MESHD ( COVID-19 MESHD), is now pandemic with nearly three million cases reported to date1. Although the majority of COVID-19 MESHD patients experience only mild or moderate symptoms, a subset will progress to severe disease with pneumonia MESHD and acute respiratory distress syndrome MESHD ( ARDS MESHD) requiring mechanical ventilation2. Emerging results indicate a dysregulated MESHD immune response characterized by runaway inflammation MESHD, including cytokine release syndrome (CRS), as the major driver of pathology in severe COVID-19 MESHD3,4. With no treatments currently approved for COVID-19 MESHD, therapeutics to prevent or treat the excessive inflammation MESHD in severe disease caused by SARS-CoV-2 infection MESHD are urgently needed. Here, in 10 terminally-ill, critical COVID-19 MESHD patients we report profound elevation of plasma IL-6 HGNC and CCL5 HGNC ( RANTES HGNC), decreased CD8 HGNC+ T cell levels, and SARS-CoV-2 plasma viremia MESHD. Following compassionate care treatment with the CCR5 HGNC blocking antibody leronlimab, we observed complete CCR5 HGNC receptor occupancy on macrophage and T cells, rapid reduction of plasma IL-6 HGNC, restoration of the CD4 HGNC/ CD8 HGNC ratio, and a significant decrease in SARS-CoV-2 plasma viremia MESHD. Consistent with reduction of plasma IL-6 HGNC, single-cell RNA-sequencing revealed declines MESHD in transcriptomic myeloid cell clusters expressing IL-6 HGNC and interferon-related genes. These results demonstrate a novel approach to resolving unchecked inflammation MESHD, restoring immunologic deficiencies MESHD, and reducing SARS-CoV-2 plasma viral load via disruption of the CCL5 HGNC- CCR5 HGNC axis, and support randomized clinical trials to assess clinical efficacy of leronlimab-mediated inhibition of CCR5 HGNC for COVID-19 MESHD.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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