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HGNC Genes

SARS-CoV-2 proteins

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    The type 2 asthma mediator IL-13 inhibits SARS-CoV-2 infection MESHD of bronchial epithelium

    Authors: Luke R Bonser; Walter L Eckalbar; Lauren Rodriguez; Jiangshan Shen; Kyung Duk Koh; Lorna T Zlock; Stephanie Christenson; Prescott G Woodruff; Walter E Finkbeiner; David J Erle

    doi:10.1101/2021.02.25.432762 Date: 2021-02-25 Source: bioRxiv

    Rationale: Asthma is associated with chronic changes in the airway epithelium, a key target of SARS-CoV-2. Many epithelial changes are driven by the type 2 cytokine IL-13 HGNC, but the effects of IL-13 HGNC on SARS-CoV-2 infection MESHD are unknown. Objectives: We sought to discover how IL-13 HGNC and other cytokines affect expression of genes encoding SARS-CoV-2-associated host proteins in human bronchial epithelial cells (HBECs) and determine whether IL-13 HGNC stimulation alters susceptibility to SARS-CoV-2 infection MESHD. Methods: We used bulk and single cell RNA-seq to identify cytokine-induced changes in SARS-CoV-2-associated gene expression in HBECs. We related these to gene expression changes in airway epithelium from individuals with mild-moderate asthma MESHD and chronic obstructive pulmonary disease MESHD ( COPD MESHD). We analyzed effects of IL-13 HGNC on SARS-CoV-2 infection MESHD of HBECs. Measurements and Main Results: Transcripts encoding 332 of 342 (97%) SARS-CoV-2-associated proteins were detected in HBECs ([≥]1 RPM in 50% samples). 41 (12%) of these mRNAs were regulated by IL-13 HGNC (>1.5-fold change, FDR < 0.05). Many IL-13 HGNC-regulated SARS-CoV-2-associated genes were also altered in type 2 high asthma and COPD MESHD. IL-13 HGNC pretreatment reduced viral RNA recovered from SARS-CoV-2 infected MESHD cells and decreased dsRNA, a marker of viral replication, to below the limit of detection in our assay. Mucus also inhibited viral infection MESHD. Conclusions: IL-13 HGNC markedly reduces susceptibility of HBECs to SARS-CoV-2 infection MESHD through mechanisms that likely differ from those activated by type I interferons. Our findings may help explain reports of relatively low prevalence of asthma MESHD in patients diagnosed with COVID-19 MESHD and could lead to new strategies for reducing SARS-CoV-2 infection MESHD.

    Type 2 and interferon inflammation strongly regulate SARS-CoV-2 related gene expression in the airway epithelium

    Authors: Satria P Sajuthi; Peter DeFord; Nathan D Jackson; Michael T Montgomery; Jamie L Everman; Cydney L Rios; Elmar Pruesse; James D Nolin; Elizabeth G Plender; Michael E Wechsler; Angel CY Mak; Celeste Eng; Sandra Salazar; Vivian Medina; Eric M Wohlford; Scott Huntsman; Deborah A Nickerson; Soren Germer; Michael C Zody; Goncalo Abecasis; Hyun Min Kang; Kenneth M Rice; Sam Oh; Jose Rodriguez-Santana; Esteban G Burchard; Max A Seibold

    doi:10.1101/2020.04.09.034454 Date: 2020-04-10 Source: bioRxiv

    Coronavirus disease 2019 MESHD ( COVID-19 MESHD) outcomes vary from asymptomatic infection to death. This disparity may reflect different airway levels of the SARS-CoV-2 receptor, ACE2 HGNC, and the spike protein PROTEIN activator, TMPRSS2 HGNC. Here we explore the role of genetics and co-expression networks in regulating these genes in the airway, through the analysis of nasal airway transcriptome data from 695 children. We identify expression quantitative trait loci (eQTL) for both ACE2 HGNC and TMPRSS2 HGNC, that vary in frequency across world populations. Importantly, we find TMPRSS2 HGNC is part of a mucus secretory network, highly upregulated by T2 inflammation MESHD through the action of interleukin-13 HGNC, and that interferon response to respiratory viruses highly upregulates ACE2 HGNC expression. Finally, we define airway responses to coronavirus infections MESHD in children, finding that these infections upregulate IL6 HGNC while also stimulating a more pronounced cytotoxic immune response relative to other respiratory viruses. Our results reveal mechanisms likely influencing SARS-CoV-2 infectivity MESHD and COVID-19 MESHD clinical outcomes.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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