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    Overactive EGFR Signaling Leads to Lung Fibrosis After SARS-CoV Infection

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    Author
    Venkataraman, Thiagarajan
    0000-0003-0921-6345
    Advisor
    Frieman, Matthew B.
    Date
    2017
    Type
    dissertation
    
    Metadata
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    Abstract
    SARS coronavirus (SARS-CoV) is a pathogenic respiratory virus that causes acute lung injury in humans. In turn, the host mounts a wound healing response to repair the injury. One of the major sequelae caused by SARS-CoV is pulmonary fibrosis (PF), which occurs more frequently in older patients. Fibrosis is caused by a dysregulated wound healing response and the molecular pathways underlying the development of fibrosis are not completely understood. Using mouse models of SARS-CoV pathogenesis, we have identified that the wound healing pathway, controlled by the epidermal growth factor receptor (EGFR) is critical to recovery from SARS-CoV induced tissue damage. In mice with constitutively active EGFR, [EGFR(DSK5) mice], we find that SARS-CoV infection causes enhanced lung disease. Importantly, we show that during infection the EGFR ligands amphiregulin and HB-EGF are upregulated and exogenous addition of these ligands during infection of wildtype mice leads to enhanced lung disease and altered wound healing dynamics. Our data demonstrate a key role of EGFR in the host response to SARS-CoV and how it may be implicated in lung disease induced by other highly pathogenic respiratory viruses.
    Description
    University of Maryland, Baltimore. Molecular Microbiology and Immunology. Ph.D. 2017
    Keyword
    EGFR
    HB-EGF
    SARS-CoV
    Amphiregulin
    Fibrosis
    Heparin-binding EGF-like Growth Factor
    SARS Virus
    Wound Healing
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/6731
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    Theses and Dissertations School of Medicine
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