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SARS-CoV-2 proteins

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    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.

    C-C chemokine receptor type 5 links COVID-19 MESHD, Rheumatoid arthritis, and Hydroxychloroquine: In silico analysis 

    Authors: MAHMOOD Yaseen HACHIM; Ibrahim Hachim; Kashif Naeem; Haifa Hannawi; Issa Al Salmi; Suad Hannawi

    doi:10.21203/rs.3.rs-48001/v2 Date: 2020-07-23 Source: ResearchSquare

    Patients with r heumatoid arthritis MESHD(R A) MESHD represent one of the fragile patient groups that might be susceptible to the critical form of the coronavirus disease -19 ( COVID-19 MESHD) . On the other side, R A MESHDpatients have been found not to have an increased risk of COVID-19 MESHD OVID-19 infection. MESHD Moreover, some of the Disease-Modifying Anti-Rheumatic Drugs (DMARDS)  commonly used to treat r heumatic diseases MESHDlike Hydroxychloroquine (HCQ) were proposed as a potential therapy for COVID-19 MESHD  with a lack of full understanding of their molecular mechanisms. This highlights the need for the discovery of common pathways that may link both diseases at the molecular side. In this research, we used the in silico approach to investigate the transcriptomic profile of R A MESHDsynovium to identify shared molecular pathways with that of severe acute r espiratory syndrome-corona virus-2 (SARS-COV-2) infected lung MESHDtissue. Our results showed upregulation of chemotactic factors, including C CL4, HGNC C CL8, HGNC and C CL11, HGNC that all shared C CR5 HGNCas their receptor, as a common derangement observed in both diseases; R A MESHDand COVID-19 MESHD. Moreover, our results also highlighted a possible mechanism through which HCQ, which can be used as a monotherapy in mild R A MESHDor as one of the triple-DMARDs therapy (tDMARDs; methotrexate, sulphasalazine, and HCQ), might interfere with the COVID-19 MESHD i nfection. MESHD This might be achieved through the ability of HCQ to upregulate specific immune cell populations like activated natural killer (NK) cells, which were found to be significantly reduced in COVID-19 MESHD i nfection. MESHD In addition to its ability to block C CR5 HGNCrich immune cell recruitment that also was upregulated in the S ARS-COV-2 infected lungs. MESHD This might explain some of the reports that showed beneficial effects. 

    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.

    C-C Chemokine Receptor Type 5 HGNC Links COVID-19 MESHD, Rheumatoid Arthritis, and Hydroxychloroquine

    Authors: Mahmood Yaseen HACHIM; Ibrahim Y. Hachim; Kashif Naeem; Haifa Hannawi; Issa Al Salmi; Suad Hannawi

    doi:10.21203/rs.3.rs-37404/v1 Date: 2020-06-22 Source: ResearchSquare

    Background: Patients with rheumatoid arthritis MESHD ( RA MESHD) represent one of the fragile patient groups that might be susceptible to coronavirus disease -19 ( COVID-19 MESHD) and its severe form. On the other side, RA MESHD patients have been found not to have an increased risk of COVID19 MESHD infection. Moreover, some of the Disease-Modifying Anti-Rheumatic Drugs (DMARDS)  commonly used to treat rheumatic diseases MESHD like Hydroxychloroquine (HCQ) were proposed as a potential therapy for COVID19 MESHD with a lack of full understanding of their molecular mechanisms. This highlights the need for the discovery of common pathways that may link both diseases at the molecular side Methods: We used the in silico approach to investigate the transcriptomic profile of RA MESHD synovium compared to osteoarthritis MESHD and healthy controls to identify RA MESHD specific molecular pathways shared with that of severe acute respiratory syndrome-corona virus-2 (SARS-COV-2) infected lung MESHD tissue. Results: Our results showed upregulation of chemotactic factors, including CCL4 HGNC, CCL8 HGNC, and CCL11 HGNC, that all shared CCR5 HGNC as their receptor, as a common derangement observed in both diseases; RA MESHD and COVID-19 MESHD. Moreover, our results also highlighted that HCQ might interfere with the COVID-19 MESHD infection through its ability to upregulate specific immune cell populations like activated natural killer (NK) cells, besides blocking CCR5 HGNC rich immune cell recruitment to the SARS-COV-2 infected MESHD lungs Conclusion: Our results might explain some of the reports that showed beneficial effects and indicate the need for proper patients stratification on their immune profile before selecting the therapeutic protocol or clinical trial enrollment. Keyword COVID-19 MESHD, SARS-COV-2, Hydroxychloroquine, rheumatoid arthritis MESHD

    SARS-CoV-2 activates lung epithelia cell proinflammatory signaling and leads to immune dysregulation in COVID-19 MESHD patients by single-cell sequencing

    Authors: Huarong Chen; Weixin Liu; Dabin Liu; Liuyang Zhao; Jun Yu

    doi:10.1101/2020.05.08.20096024 Date: 2020-05-13 Source: medRxiv

    Objective: The outbreak of Coronavirus disease 2019 MESHD ( COVID-19 MESHD) caused by SARS-CoV-2 infection MESHD has become a global health emergency. We aim to decipher SARS-CoV-2 infected MESHD cell types, the consequent host immune response and their interplay in the lung of COVID-19 MESHD patients. Design: We analyzed single-cell RNA sequencing (scRNA-seq) data of lung samples from 17 subjects (6 severe COVID-19 MESHD patients, 3 mild patients who recovered and 8 healthy controls). The expression of SARS-CoV-2 receptors ( ACE2 HGNC and TMPRSS2 HGNC) was examined among different cell types in the lung. The immune cells infiltration patterns, their gene expression profiles, and the interplay of immune cells and SARS-CoV-2 target cells were further investigated. Results: Compared to healthy controls, the overall ACE2 HGNC (receptor of SARS-CoV-2) expression was significantly higher in lung epithelial cells of COVID-19 MESHD patients, in particular in ciliated cell, club cell and basal cell. Comparative transcriptome analysis of these lung epithelial cells of COVID-19 MESHD patients and healthy controls identified that SARS-CoV-2 infection MESHD activated pro-inflammatory signaling including interferon pathway and cytokine signaling. Moreover, we identified dysregulation of immune response in patients with COVID-19 MESHD. In severe COVID-19 MESHD patients, significantly higher neutrophil, but lower T and NK cells in lung were observed along with markedly increased cytokines ( CCL2 HGNC, CCL3 HGNC, CCL4 HGNC, CCL7 HGNC, CCL3L1 HGNC and CCL4L2 HGNC) compared with healthy controls as well as mild patients who recovered. The cytotoxic phenotypes were shown in lung T and NK cells of severe patients as evidenced by enhanced IFN{gamma HGNC}, Granulysin HGNC, Granzyme B HGNC and Perforin expression. Moreover, SARS-CoV-2 infection MESHD altered the community interplay of lung epithelial cells and immune cells: the interaction between epithelial cells with macrophage, T and NK cell was stronger, but their interaction with neutrophils was lost in COVID-19 MESHD patients compared to healthy controls. Conclusions: SARS-CoV-2 infection MESHD activates pro-inflammatory signaling in lung epithelial cells expressing ACE2 HGNC and causes dysregulation of immune response to release more pro-inflammatory cytokines. Moreover, SARS-CoV-2 infection MESHD breaks the interplay of lung epithelial cells and immune cells.

    Lysosomotropic Active Compounds—Hidden Protection against COVID-19 MESHD / SARS-CoV-2 Infection MESHD?

    Authors: Markus Blaess; Lars Kaiser; Martin Sauer; Hans-Peter Deigner

    id:10.20944/preprints202005.0061.v1 Date: 2020-05-05 Source: Preprints.org

    The COVID-19 MESHD COVID-19 MESHD pandemic is one of the largest challenges in medicine and health care worldwide in recent decades, and it is infecting and killing increasing numbers of people every day. In this paper, we discuss the possible relationships among lysosomotropism, increasing lysosomal pH, and the SARS-CoV-2 infection MESHD and disease process, and we deduce a possible approach for treatment and prophylaxis. Lysosomotropism is a biological characteristic of small molecules, such as (hydroxyl)chloroquine, amitriptyline, NB 06, or sertraline, which is present in addition to intrinsic receptor-mediated or enzymatic pharmacological effects. Lysosomotropic compounds affect prominent inflammatory messengers, such as IL1B HGNC, CCL4 HGNC, CCL20 HGNC, and IL6 HGNC, as well as cathepsin L HGNC dependent viral entry (fusion) into host cells. Therefore, this heterogeneous group of compounds is a promising candidate for the prevention and treatment of SARS-CoV-2 infections MESHD, as well as influenza A infections and cytokine release syndrome (CRS) triggered by bacterial or viral infections MESHD. Patients who have already taken medications with lysosomotropic compounds for other pre-existing conditions may benefit from this treatment in the COVID-19 pandemic MESHD. Increased lysosomal pH levels play an important role in the disease process in common skin disorders MESHD, such as psoriasis MESHD and atopic dermatitis MESHD, thus suggesting that affected individuals might benefit from their particular conditions in the COVID-19 pandemic MESHD. We suggest data analysis of patients with these diseases, and who are treated with lysosomotropic compounds, and, if the results are promising, subsequent clinical testing of off-label therapy with clinically approved lysosomotropic compounds in the current COVID-19 pandemic MESHD and future influenza A pandemics.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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