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March 2012

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From:
"Diane St. Germain" <[log in to unmask]>
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Date:
Thu, 15 Mar 2012 09:51:38 -0400
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> Dissertation Defense Announcement
> To:  The George Mason University Community
>
> Candidate: Weifeng Wang
> Program:    PhD Biosciences*
> *
> Date:   Tuesday March 20, 2012
> Time:   1:30 p.m. 
> Place:  George Mason University
>  	     Bull Run Hall, Room 258
> 	     Prince William campus <http://www.gmu.edu/resources/visitors/findex.html>*
>   
> *Dissertation Chair: Dr. Yuntao Wu
> Committee members: Dr. Daniel N. Cox, Dr. Barney Bishop, Dr. Weidong Zhou
> *
> *Title: "A dichotomy in cortical actin and chemotactic actin activity between memory and na´ve T cells
> contributes to their differential susceptibility to HIV"
>
> *
> *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 attend.
>
>
> ABSTRACT:* *
>   
>
> The persistence of viral reservoirs in HIV-infected patients impedes 
> an effective cure to AIDS. One of the major viral reservoirs in the 
> body is a small pool of latently infected CD45RO memory CD4 T cells. 
> Human memory and na´ve CD4 T cells can be identified by the reciprocal 
> expression of the CD45RO or CD45RA isoforms. In infected patients, 
> CD45RO memory CD4 T cells are preferentially infected and harbor more 
> integrated proviral DNA than CD45RA na´ve T cells. The molecular 
> mechanism dictating this differential susceptibility to HIV-1 remained 
> unknown. We discovered a phenotypic distinction between human memory 
> (CD45RO+) and na´ve (CD45RA+) resting CD4 T cells in their cortical 
> actin. Memory CD4+ T cells possess a higher cortical actin density and 
> can be distinguished as CD45RO+ Actinhigh, in contrast, naive T cells 
> are phenotypically CD45RA+Actinlow. In addition, we discovered that 
> human memory CD4+ T cells possess a lower threshold for initiating 
> signaling from CXCR4 than na´ve T cells. Low concentrations of 
> chemokine SDF-1, the natural ligand to CXCR4, predominantly induce 
> actin polymerization in memory CD4+ T cells. Furthermore, the binding 
> of HIV envelope protein gp120 to CXCR4 triggers a strong signal 
> transduction, which induces actin dynamics in memory but not na´ve 
> CD4+ T cells. The dynamic actin cytoskeleton in memory CD4+ T cell 
> promotes HIV reverse transcription and nuclei migration, which 
> facilitates to the establishment of HIV latent reservoir. We further 
> demonstrate that transient induction of actin dynamics by actin 
> modulator in resting na´ve T cells rescues HIV latent infection. These 
> results suggest a key role of chemotactic actin activity in 
> facilitating HIV-1 latent infection of these T cell subsets.
>
> ###
>


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