XIX International AIDS Conference


TUAA02 Mechanism of HIV Latency
  Oral Abstract Session : Track A
Venue: Session Room 2
Time: 24.07.2012, 16:30 - 18:00
Co-Chairs: Warner Greene, United States
Carine Van Lint, Belgium
 
 

16:30
TUAA0201
Abstract
Powerpoint
Webcast
Unique regulatory mechanisms of CNS-derived HIV-1 LTRs associated with latency
L. Gray1,2, D. Cowley1,3, E. Crespan1, C. Welsh1,4, C. Mackenzie1,5, P. Gorry1,3,6, S. Wesselingh1,7, M. Churchill1,3,4
1Burnet Institute, Centre for Virology, Melbourne, Australia, 2Monash University, Department of Biochemistry and Molecular Biology, Clayton, Australia, 3Monash University, Department of Medicine, Clayton, Australia, 4Monash University, Department of Microbiology, Clayton, Australia, 5Monash University, Department of Immunology, Melbourne, Australia, 6The University of Melbourne, Department of Microbiology and Immunology, Melbourne, Australia, 7South Australian Health and Medical Research Institute, Adelaide, Australia
L. Gray, Australia

16:45
TUAA0202
Abstract
Webcast
Complete transcriptome analysis of latently infected CD4+ T cells
M. Iglesias-Ussel1, L. Marchionni2, F. Romerio1
1University of Maryland School of Medicine, Institute of Human Virology, Baltimore, United States, 2Johns Hopkins University, Sidney Kimmel Comprehensive Cancer Center, Baltimore, United States
F. Romerio, United States

17:00
TUAA0203
Abstract
Powerpoint
Webcast
CBF-1 induces both establishment and maintenance of HIV latency via recruiting PcG corepressor complex at LTR
M. Tyagi
George Mason University, Manassas, United States
M. Tyagi, United States

17:15
TUAA0204
Abstract
Webcast
Epigenetic modifications of HIV proviral LTRs: potential targets for cure
S. Weber1, H. Burger2, K. Kemal2, B. Weiser2, K. Korn1, K. Anastos3, W. Doerfler1
1Erlangen University, Institute for Virology, Erlangen, Germany, 2Wadsworth Center, New York State Dept. of Health, Albany, United States, 3Albert Einstein College of Medicine/ Montefiore Medical Center, New York, United States
S. Weber, Germany

17:30
TUAA0205
Abstract
Powerpoint
Webcast
Unique integration patterns: in vitro model of HIV latency
S. Saleh1,2, D. Vatakis3, P. Cameron1,2,4, A. Harman5, A. Cunningham5, S. Lewin1,2,4
1Monash University, Medicine, Melbourne, Australia, 2Burnet Institute, Melbourne, Australia, 3University of California at Los Angeles, Medicine, Los Angeles, United States, 4Infectious Diseases Unit, Alfred Hospital, Melbourne, Australia, 5Westmead Millenium Institute, Sydney, Australia
S. Saleh, Australia

Powerpoints presentations
Unique regulatory mechanisms of CNS-derived HIV-1 LTRs associated with latency - Lachlan Gray

CBF-1 induces both establishment and maintenance of HIV latency via recruiting PcG corepressor complex at LTR - Mudit Tyagi
CBF-1 induces both establishment and maintenance of HIV latency via recruiting PcG corepressor complex at LTR - Mudit Tyagi

Unique integration patterns: in vitro model of HIV latency - Suha Saleh



Rapporteur report

Track A report by Jason Brenchley


The theme of this session was the study of  mechanisms underlying maintenance of latency in HIV-infected cells. Dr. Lachlan Gray (Burnet Institute) discussed mechanisms controlling HIV latency that are specific to the central nervous system. He found decreased transcriptional activity of HIV within CNS, which was associated with expression of the transcriptional repressor Sp3, in contrast to Sp1 which is a more canonical binder to the HIV LTR. Dr. Fabio Romerio (University of Maryland) performed transcriptional analysis using an in vitro model of latent HIV infection of peripheral blood CD4 T cells. Several transcriptional differences were found between uninfected cells and cells latently HIV infected. These differences suggested that HIV may exploit cellular suppression functions to maintain latency. Dr. Mudit Tyagi (George Mason University) discussed induction and maintenance of latency in HIV-infected primary CD4 T cells and transformed cell lines by recruitment of PcG repressor to the locus of HIV integration. Dr. Tyagi found that CBF-1 can induce repressive chromatin structure by recruiting Polycomb Group corepressors to the HIV LTR. Dr.Stefanie Weber (Erlangen University) discussed epigenetic modifications which occur to the HIV LTR and unexpectedly found LTR-located CpG dinucleotides being mutated. These specific LTR mutations were speculated to be targets of therapeutic interventions. Dr. Suha Saleh (Monash University) discussed unique integration site patterns in peripheral blood CD4 T cells experimentally infected with HIV.  Dr. Saleh found that integration sites of HIV were influenced by the mechanisms by which the CD4 T cells were stimulated, but HIV tended to integrate in transcriptionally active genes. Following the presentations discussion noted that further studies might focus on understanding HIV latency in vivo, but the difficulty in retrieving sufficient latently-infected cells from in vivo reservoirs was mentioned. 




   

    The organizers reserve the right to amend the programme.


Contact Us | Site map © 2012 International AIDS Society