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Overactive EGFR Signaling Leads to L...

Venkataraman, Thiagarajan.

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

Record Type:	Electronic resources : Monograph/item
Title/Author:	Overactive EGFR Signaling Leads to Lung Fibrosis After SARS-CoV Infection./
Author:	Venkataraman, Thiagarajan.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2017,
Description:	143 p.
Notes:	Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.
Contained By:	Dissertation Abstracts International78-10B(E).
Subject:	Virology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10259261
ISBN:	9781369822786

Overactive EGFR Signaling Leads to Lung Fibrosis After SARS-CoV Infection.
Venkataraman, Thiagarajan.

Overactive EGFR Signaling Leads to Lung Fibrosis After SARS-CoV Infection. - Ann Arbor : ProQuest Dissertations & Theses, 2017 - 143 p.

Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.

Thesis (Ph.D.)--University of Maryland, Baltimore, 2017.

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.

ISBN: 9781369822786Subjects--Topical Terms:

642304
Virology.

Overactive EGFR Signaling Leads to Lung Fibrosis After SARS-CoV Infection.
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520 $a 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.
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