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MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ORF8 (2)

ProteinS (2)


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SARS-CoV-2 Proteins
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    The Discovery of a Recombinant SARS2-like CoV Strain Provides Insight Into SARS and COVID-19 MESHD Pandemics

    Authors: Xin Li; Xiufeng Jin; Shunmei Chen; Liangge Wang; Tung On Yau; Jianyi Yang; Zhangyong Hong; Jishou Ruan; Guangyou Duan; Shan Gao

    doi:10.21203/rs.3.rs-60430/v1 Date: 2020-08-16 Source: ResearchSquare

    Background: In December 2019, the world awoke to a new zoonotic strain of coronavirus named severe acute respiratory syndrome coronavirus-2 MESHD (SARS-CoV-2).Results: In the present study, we classified betacoronavirus subgroup B into the SARS-CoV-2, SARS-CoV MESHD and SARS-like CoV clusters, and the ORF8 PROTEIN genes of these three clusters into types 1, 2 and 3, respectively. One important result of our study is that we reported—for the first time—a recombination event of ORF8 PROTEIN at the whole-gene level in a bat, which had been co-infected MESHD by two betacoronavirus strains. This result provides substantial proof for long-existing hypotheses regarding the recombination and biological functions of ORF8 PROTEIN. Based on the analysis of recombination events in the Spike gene, we propose that the Spike protein PROTEIN of SARS-CoV-2 may have more than one specific receptor for its function as gp120 HGNC of HIV has CD4 HGNC and CCR5 HGNC. In the present study, we also found that the ancestor of betacoronavirus had a strong first Internal Ribosome Entry Site (IRES) and at least one furin cleavage site (FCS) in the junction region between S1 and S2 subunits.Conclusions: We concluded that the junction FCS in SARS-CoV-2 may increase the efficiency of its entry into cells, while the type 2 ORF8 PROTEIN acquired by SARS-CoV may increase its replication efficiency. These two most critical events provide the most likely explanation for SARS and COVID-19 pandemic MESHD COVID-19 pandemic MESHDs.

    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. 

    The discovery of a recombinant SARS2-like CoV strain provides insights into SARS and COVID-2019 pandemics

    Authors: Xin Li; Xiufeng Jin; Shunmei Chen; Liangge Wang; Tung On Yau; Jianyi Yang; Zhangyong Hong; Jishou Ruan; Guangyou Duan; Shan Gao

    doi:10.1101/2020.07.22.213926 Date: 2020-07-22 Source: bioRxiv

    In December 2019, the world awoke to a new zoonotic strain of coronavirus named severe acute respiratory syndrome coronavirus-2 MESHD (SARS-CoV-2). In the present study, we classified betacoronavirus subgroup B into the SARS-CoV-2, SARS-CoV MESHD and SARS-like CoV clusters, and the ORF8 PROTEIN genes of these three clusters into types 1, 2 and 3, respectively. One important result of our study is that the recently reported strain RmYN02 was identified as a recombinant SARS2-like CoV strain that belongs to the SARS-CoV-2 cluster MESHD, but has an ORF8 PROTEIN from a SARS-like CoV. This result provides substantial proof for long-existing hypotheses regarding the recombination and biological functions of ORF8 PROTEIN. Based on the analysis of recombination events in the Spike gene, we propose that the Spike protein PROTEIN of SARS-CoV-2 may have more than one specific receptor for its function as gp120 HGNC of HIV has CD4 HGNC and CCR5 HGNC. We concluded that the furin protease cleavage site acquired by SARS-CoV-2 may increase the efficiency of viral entry into cells, while the type 2 ORF8 PROTEIN acquired by SARS-CoV may increase its replication efficiency. These two most critical events provide the most likely explanation for SARS and COVID-2019 pandemics.

    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

    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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