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HGNC Genes

SARS-CoV-2 proteins

ProteinS (1)


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    Genome-wide bioinformatic analyses predict key host and viral factors in SARS-CoV-2 pathogenesis

    Authors: Mariana Ferrarini; Avantika Lal; Rita Rebollo; Andreas Gruber; Andrea Guarracino; Itziar Martinez Gonzalez; Taylor Floyd; Daniel Siqueira de Oliveira; Justin Shanklin; Ethan Beausoleil; Taneli Pusa; Brett Pickett; Vanessa Aguiar-Pulido

    doi:10.21203/rs.3.rs-63136/v1 Date: 2020-08-20 Source: ResearchSquare

    The novel betacoronavirus named Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) caused a worldwide pandemic ( COVID-19 MESHD) after initially emerging in Wuhan, China. Here we applied a novel, comprehensive bioinformatic strategy to public RNA sequencing and viral genome sequencing data, to better understand how SARS-CoV-2 interacts with human cells. To our knowledge, this is the first meta-analysis to predict host factors that play a specific role in SARS-CoV-2 pathogenesis, distinct from other respiratory viruses. We identified differentially expressed genes, isoforms and transposable element families specifically altered in SARS-CoV-2 infected MESHD cells. Well-known immunoregulators including CSF2 HGNC, IL-32 HGNC, IL-6 HGNC and SERPINA3 HGNC were differentially expressed, while immunoregulatory transposable element families were overexpressed. We predicted conserved interactions between the SARS-CoV-2 genome and human RNA-binding proteins such as hnRNPA1 HGNC, PABPC1 HGNC and eIF4b HGNC, which may play important roles in the viral life cycle. We also detected four viral sequence variants in the spike, polymerase, and nonstructural proteins that correlate with severity of COVID-19 MESHD. The host factors we identified likely represent important mechanisms in the disease profile of this pathogen, and could be targeted by prophylactics and/or therapeutics against SARS-CoV-2.

    Genome-wide bioinformatic analyses predict key host and viral factors in SARS-CoV-2 pathogenesis

    Authors: Mariana G. Ferrarini; Avantika Lal; Rita Rebollo; Andreas Gruber; Andrea Guarracino; Itziar Martinez Gonzalez; Taylor Floyd; Daniel Siqueira de Oliveira; Justin Shanklin; Ethan Beausoleil; Taneli Pusa; Brett Pickett; Vanessa Aguiar-Pulido

    doi:10.1101/2020.07.28.225581 Date: 2020-07-29 Source: bioRxiv

    The novel betacoronavirus named Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) caused a worldwide pandemic ( COVID-19 MESHD) after initially emerging in Wuhan, China. Here we applied a novel, comprehensive bioinformatic strategy to public RNA sequencing and viral genome sequencing data, to better understand how SARS-CoV-2 interacts with human cells. To our knowledge, this is the first meta-analysis to predict host factors that play a specific role in SARS-CoV-2 pathogenesis, distinct from other respiratory viruses. We identified differentially expressed genes, isoforms and transposable element families specifically altered in SARS-CoV-2 infected MESHD cells. Well-known immunoregulators including CSF2 HGNC, IL-32 HGNC, IL-6 HGNC and SERPINA3 HGNC were differentially expressed, while immunoregulatory transposable element families were overexpressed. We predicted conserved interactions between the SARS-CoV-2 genome and human RNA-binding proteins such as hnRNPA1 HGNC, PABPC1 HGNC and eIF4b HGNC, which may play important roles in the viral life cycle. We also detected four viral sequence variants in the spike, polymerase, and nonstructural proteins that correlate with severity of COVID-19 MESHD. The host factors we identified likely represent important mechanisms in the disease profile of this pathogen, and could be targeted by prophylactics and/or therapeutics against SARS-CoV-2.

    ACE2 HGNC Homo-dimerization, Human Genomic variants and Interaction of Host Proteins Explain High Population Specific Differences in Outcomes of COVID19 MESHD

    Authors: Swarkar Sharma; Inderpal Singh; Shazia Haider; Md. Zubbair Malik; Kalaiarasan Ponnusamy; Ekta Rai

    doi:10.1101/2020.04.24.050534 Date: 2020-04-24 Source: bioRxiv

    Severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2) is a positive single-stranded RNA virus that causes a highly contagious Corona Virus Disease MESHD ( COVID19 MESHD). Entry of SARS-CoV-2 in human cells depends on binding of the viral spike (S) proteins PROTEIN to cellular receptor Angiotensin-converting enzyme 2 ( ACE2 HGNC) and on S-protein PROTEIN S-protein HGNC priming by host cell serine protease TMPRSS2 HGNC. Recently, COVID19 MESHD has been declared pandemic by World Health Organization (WHO) yet high differences in disease outcomes across countries have been seen. We provide evidences to explain these population-level differences. One of the key factors of entry of the virus in host cells presumably is because of differential interaction of viral proteins with host cell proteins due to different genetic backgrounds. Based on our findings, we conclude that a higher expression of ACE2 HGNC is facilitated by natural variations, acting as Expression quantitative trait loci (eQTLs), with different frequencies in different populations. We suggest that high expression of ACE2 HGNC results in homo-dimerization, proving disadvantageous for TMPRSS2 HGNC mediated cleavage of ACE2 HGNC; whereas, the monomeric ACE2 HGNC has higher preferential binding with SARS-CoV-2 S-Protein vis MESHD S-Protein PROTEIN S-Protein HGNC vis-a-vis its dimerized counterpart. Further, eQTLs in TMPRSS2 HGNC and natural structural variations in the gene may also result in differential outcomes towards priming of viral S-protein HGNC S-protein PROTEIN, a critical step for entry of the Virus in host cells. In addition, we suggest that several key host genes, like SLC6A19 HGNC, ADAM17 HGNC, RPS6 HGNC, HNRNPA1 HGNC, SUMO1 HGNC, NACA HGNC, BTF3 HGNC and some other proteases as Cathepsins, might have a critical role. To conclude, understanding population specific differences in these genes may help in developing appropriate management strategies for COVID19 MESHD with better therapeutic interventions.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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