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    The role of epidermal growth factor receptor (EGFR) signaling in SARS coronavirus-induced pulmonary fibrosis

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    Author
    Venkataraman, T.
    Frieman, M.B.
    Date
    2017
    Journal
    Antiviral Research
    Publisher
    Elsevier B.V.
    Type
    Article
    
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    See at
    https://doi.org/10.1016/j.antiviral.2017.03.022
    Abstract
    Many survivors of the 2003 outbreak of severe acute respiratory syndrome (SARS) developed residual pulmonary fibrosis with increased severity seen in older patients. Autopsies of patients that died from SARS also showed fibrosis to varying extents. Pulmonary fibrosis can be occasionally seen as a consequence to several respiratory viral infections but is much more common after a SARS coronavirus (SARS-CoV) infection. Given the threat of future outbreaks of severe coronavirus disease, including Middle East respiratory syndrome (MERS), it is important to understand the mechanisms responsible for pulmonary fibrosis, so as to support the development of therapeutic countermeasures and mitigate sequelae of infection. In this article, we summarize pulmonary fibrotic changes observed after a SARS-CoV infection, discuss the extent to which other respiratory viruses induce fibrosis, describe available animal models to study the development of SARS-CoV induced fibrosis and review evidence that pulmonary fibrosis is caused by a hyperactive host response to lung injury mediated by epidermal growth factor receptor (EGFR) signaling. We summarize work from our group and others indicating that inhibiting EGFR signaling may prevent an excessive fibrotic response to SARS-CoV and other respiratory viral infections and propose directions for future research.
    Keyword
    EGFR
    Fibrosis
    SARS-CoV
    Wound healing
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85018490378&doi=10.1016%2fj.antiviral.2017.03.022&partnerID=40&md5=cb73aed3e046ecc12e7743ef2bc0d331; http://hdl.handle.net/10713/12399
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.antiviral.2017.03.022
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