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March 2016

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Subject:
From:
"Diane St. Germain" <[log in to unmask]>
Reply To:
Diane St. Germain
Date:
Mon, 21 Mar 2016 14:52:31 +0000
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Thesis Defense Announcement
To:  The George Mason University Community

Candidate: Taryn Brooks-Faulconer

Program: M.S. in Biology



Date:   Monday April 4, 2016

Time:   10:00 am

Place:  George Mason University
             Science & Technology Campus<http://www.gmu.edu/resources/welcome/Directions-to-GMU.html>

             Bull Run Hall, Room 131



Title: "Altered Mitochondrial Dynamics in Venezuelan Equine Encephalitis Virus Infected Cells"
Thesis Director: Dr. Aarthi Narayanan
Thesis Committee:  Dr. Kylene Kehn-Hall, Dr. Ancha Baranova
A copy of the thesis will be available in the Gateway Library.  All are invited to attend the defense.
ABSTRACT
To establish productive infection, viruses profoundly alter both the intracellular environment and the cellular function. Mitochondria are critically important cellular organelles that generate energy and ensure cell survival. Mitochondria are also crucial for innate immunity response as they serve as the sentinels that sense infection and initiate host responses. For many viruses, the changes in mitochondrial dynamics were documented to occur early in infection. Venezuelan Equine Encephalitis Virus (VEEV) is a New World alphavirus that infects neuronal cells and produces an encephalitic phenotype. In this manuscript, we demonstrate that VEEV infection results in mitochondrial alterations that include changes in the morphology and intracellular distribution of mitochondria, reduction in mitochondrial membrane potential and localization of their enzymatic components. In particular, we report perinuclear accumulation of mitochondria in infected cells and partial co-localization of the viral capsid proteins with mitochondrial membranes. The pronounced changes to the mitochondria observed in VEEV infected cells probably play a role in the development of the virus-specific cytopathic effects. Our studies demonstrate that the mitochondria are critical intracellular platforms affected by alphavirus infections.
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