January 2010


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To: Biology Graduate Students <[log in to unmask]>, Biosciences Graduate Students <[log in to unmask]>, Anna Baranova <[log in to unmask]>, Daniel N Cox <[log in to unmask]>, Alan H Christensen <[log in to unmask]>, Chip Petricoin <[log in to unmask]>, Geraldine M Grant <[log in to unmask]>, Karl J Fryxell <[log in to unmask]>, Monique Van Hoek <[log in to unmask]>, Yuntao Wu <[log in to unmask]>, Charles L Bailey <[log in to unmask]>, Jim Willett <[log in to unmask]>, Serguei Popov <[log in to unmask]>, Lance Liotta <[log in to unmask]>, Valery Soyfer <[log in to unmask]>, Kylene Kehn-Hall <[log in to unmask]>, Fatah Kashanchi <[log in to unmask]>, Barney M Bishop <[log in to unmask]> cc: "Gail L. Hodges" <[log in to unmask]>, Sarah Kostka <[log in to unmask]>
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"Diane St. Germain" <[log in to unmask]>
Fri, 8 Jan 2010 15:40:59 -0500
George Mason University
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*Dissertation Defense Announcement:
To:  The George Mason University Community*

*Jeremy Kelly
PhD Biosciences Candidate
*Date:   Friday, January 15, 2010
Time:   10:00 a.m. 
Place:  George Mason University, Prince William campus
	     Discovery Hall Auditorium 
Dissertation Chair: Dr. Yuntao Wu

Title: **"HIV Initiates Multiple Signaling Cascades Required for Effective Replication"**


*A copy of the dissertation is on reserve in the Johnson Center Library, 
Fairfax campus.  The doctoral project will not be read at the meeting, 
but should be read in advance. *

*All members of the George Mason University community are invited to 


The Human Immunodeficiency Virus (HIV) infects lymphocytes by binding
to CD4 and either the CXCR4 or CCR5 receptor. Signaling initiated by
these receptors in response to the virus was originally found to be
unnecessary for viral infection.  However, recent work by our lab has
demonstrated that in resting CD4 T cells CXCR4 signaling is necessary
to overcome cortical actin restriction.  Here we show that multiple
signaling cascades are not only initiated by HIV and CD4/CXCR4
signaling, but that this signaling can impact viral replication in
non-resting cells. We specifically identify the JAK/STAT pathway as a
necessary component of early viral transcription; which has
implications for not only novel therapeutics but also for
understanding how we view viral interactions with the immune system.