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This article is part of the supplement: 15th International Conference on Human Retroviruses: HTLV and Related Viruses

Open Access Open Badges Meeting abstract

Varying modulation of HTLV-1 LTR activity by BAF complexes

Rachel Van Duyne12, Irene Guendel1, Nazly Shafagati1, Kylene Kehn-Hall1, Rebecca Easley1, Zachary Klase3, Sergei Nekhai4, Mudit Tyagi1 and Fatah Kashanchi12*

Author Affiliations

1 George Mason University, Department of Molecular and Microbiology, National Center for Biodefense and Infectious Diseases, Manassas, VA, 20110, USA

2 The George Washington University Medical Center, Department of Microbiology, Immunology, and Tropical Medicine, Washington, DC, 20037, USA

3 National Institutes of Health, Molecular Virology Section, Laboratory of Molecular Microbiology, NIAID, Bethesda, Maryland, 20892, USA

4 Howard University, Department of Microbiology, Center for Sickle Cell Disease, Department of Medicine, Washington DC, 20060, USA

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Retrovirology 2011, 8(Suppl 1):A180  doi:10.1186/1742-4690-8-S1-A180

The electronic version of this article is the complete one and can be found online at:

Published:6 June 2011

© 2011 Van Duyne et al; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Meeting abstract

Chromatin remodeling is a rapidly emerging field with critical implications for the control of viral gene expression, especially for viruses with integrated genomes, such as HTLV-1. Recent observations indicate that there are as many as eight different BRG1 containing chromatin remodeling complexes highlight the advancement in the field, but also the necessity for future study especially when looking at viral infections. In the current study we focused on few of the Baf subunits that are common to most SWI/SNF complexes. We find that at least three Bafs, Baf53, Baf155 and Baf170, are highly regulated in HTLV-1 infected cells. Along these lines others have shown that depletion of Baf53 leads to the expansion of chromosome territories and decompaction of the chromatin. Here we show that there are clear varying differences between the Baf subunits after viral infection. These subunits also co-elute in different places from a sizing column and one particular form, Baf53 may be phosphorylated in HTLV-1 infected cells. Normally Baf53 is a suppressive complex and knock down experiments show increased level of virus gene expression from transfected or chronically infected cells.