Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (2)

ProteinN (1)


SARS-CoV-2 Proteins
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    Resistance of endothelial cells to SARS-CoV-2 infection MESHD in vitro

    Authors: Blerina Ahmetaj-Shala; Thomas P Peacock; Laury Baillon; Olivia Swann; Hime Gashaw; Wendy S Barclay; Jane A. Mitchell; Chiara Piubelli; Greta Bergamaschi; Marcella Chiari; Alessandro Gori; Marina Cretich

    doi:10.1101/2020.11.08.372581 Date: 2020-11-09 Source: bioRxiv

    Rationale: The secondary thrombotic MESHD/vascular clinical syndrome of COVID-19 MESHD suggests that SARS-CoV-2 infects MESHD not only respiratory epithelium but also the endothelium activating thrombotic MESHD pathways, disrupting barrier function and allowing access of the virus to other organs of the body. However, a direct test of susceptibility to SARS-CoV-2 of authentic endothelial cell lines has not been performed. Objective: To determine infectibility of primary endothelial cell lines with live SARS-CoV-2 and pseudoviruses expressing SARS-CoV-2 spike PROTEIN protein. Methods and Results: Expression of ACE2 HGNC and BSG pathways genes was determined in three types of endothelial cells; blood outgrowth, lung microvascular and aortic endothelial cells. For comparison nasal epithelial cells, Vero E6 cells (primate kidney fibroblast cell line) and HEK 293T cells (human embryonic kidney cells) transfected with either ACE2 HGNC or BSG were used as controls. Endothelial and Vero E6 cells were treated with live SARS-CoV-2 virus for 1 hour and imaged at 24 and 72 hours post infection. Pseudoviruses containing SARS-CoV-2, Ebola and Vesicular Stomatis Virus MESHD glycoproteins were generated and added to endothelial cells and HEK 239Ts for 2 hours and infection measured using luminescence at 48 hours post infection. Compared to nasal epithelial cells, endothelial cells expressed low or undetectable levels of ACE2 HGNC and TMPRSS2 HGNC but comparable levels of BSG, PPIA HGNC and PPIB HGNC. Endothelial cells showed no susceptibility to live SARS-CoV-2 or SARS-CoV-2 pseudovirus (but showed susceptibility to Ebola and Vesicular Stomatitis Virus MESHD). Overexpression of ACE2 HGNC but not BSG in HEK 239T cells conferred SARS-CoV-2 pseudovirus entry. Endothelial cells primed with IL-1b HGNC remained resistant to SARS-CoV-2. Conclusion: Endothelial cells are resistant to infection with SARS-CoV-2 virus MESHD, in line with relatively low levels of ACE2 HGNC and TMPRSS2 HGNC, suggesting that the vascular dysfunction MESHD and thrombosis MESHD seen in severe COVID-19 MESHD is a result of factors released by adjacent infected cells (e.g. epithelial cells) and/or circulating, systemic inflammatory mediators.

    In Silico studies of Natural compounds that inhibit SARS-CoV-2 Nucleocapsid Nsp1 HGNC/ Nsp3 HGNC proteins mediated Viral Replication and Pathogenesis

    Authors: Hemanth Kumar Manikyam

    doi:10.21203/ Date: 2020-11-05 Source: ResearchSquare

    Highly Transmissible and pathogenic coronavirus that emerged in late December of 2019 caused Severe acute respiratory syndrome MESHD (SARS-CoV-2), which challenged human health and public safety. Severity of the disease depends on the viral load and the type of mutation that occurred in the coronavirus. Nonstructural proteins like, Nsp1 HGNC, Nsp3 HGNC, Nsp12 and Nsp13 including other viral proteins plays important role during viral replication life cycle. Viral Replication initiated by hacking the host cellular mechanism either by synergy or by suppression using nucleocapsid proteins PROTEIN of the virus. Spike (S) protein PROTEIN of the SARS-CoV-2 uses angiotensin-converting enzyme II ( ACE2 HGNC) and TRMPSS as a cell entry. Once virus enters host cell, nucleocapsid proteins PROTEIN along with its genome is releases from endosomes into cytosol of the host cell. Ca2+/ CaM HGNC ( Calmodulin HGNC)/Calcineurin complex of the host cell plays important role during viral replication which is mediated by nucleocapsid proteins PROTEIN of the virus. Nsp1 HGNC/ Nsp3 HGNC nonstructural proteins triggers synergetic activity with CD147 HGNC/ CyPA HGNC/ HSPG HGNC pathway and TRMP2/ADPr/Ca+2 mediated Ca2+/CaM ( Calmodulin HGNC)/Calcineurin synthesis and free radicle generation in mitochondria leading to viral replication and severe chemokine activation pathways. Docking studies were carried out to inhibit Cyclophilin A and TRMP2 proteins as drug targets. Natural compounds like Withanolide A, Columbin, Cucurbitacin E, Boswellic acid along with Cyclosporines, Vitamin E and N-Acetyl cysteine ( NAC HGNC) were selected as ligands to study docking studies. Withanolide A and Cyclosporines had shown good inhibition activity against Cyclophilin A, whereas Columbin, Boswellic acid, Cucurbitacin E, Vitamin E and N-Acetyl cysteine ( NAC HGNC) had shown inhibitory activity against TRMP2. Thus, we suggest conducting further studies to conclude above pathways mechanism and inhibitory effect of natural compounds against the Nsp1 HGNC/ Nsp3 HGNC mediated pathways Invitro and In vivo.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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