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  • Meeting abstract
  • Open Access

Human T-Lymphotropic Virus Type 1 transcription and chromatin-remodeling complexes

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  • 1, 3Email author
Retrovirology20118 (Suppl 1) :A178

  • Published:


  • Viral Protein
  • Mass Spectrometry Analysis
  • ATPase Subunit
  • Nucleosome Remodel
  • Nucleosomal Array

Human T-lymphotropic virus type 1 (HTLV-1) encodes the viral protein Tax, which is believed to act as a viral transactivator through its interactions with a variety of transcription factors, including CREB and NF- B. As is the case for all retroviruses, the provirus is inserted into the host DNA, where nucleosomes are deposited to ensure efficient packaging. Previous studies using immunoprecipitation from Tax-expressing cells, 2-dimensional gel electrophoresis, and mass spectrometry analysis have identified the ATPase subunit BRG1 as a Tax-interacting protein. BRG1, is part of at least 8 complexes which include BAF and PBAF, as well as WINAC, NCoR, mSin3A/HDAC, and NUMAC. Nucleosomes act as roadblocks in transcription, making it difficult for RNA polymerase II (Pol II) to proceed toward the 3' end of the genome. Our results using HTLV-1 integrated chromatin indicate that the Tax-activated promoter utilized PBAF complex which appears to be responsible for nucleosome remodeling. Also, the promoter was assembled into an ordered array of translationally positioned nucleosomes. In contrast, the inactive promoter was relatively inaccessible to nuclease and was not assembled into a translationally positioned nucleosomal arrays.

Authors’ Affiliations

Department of Molecular and Microbiology, National Center for Biodefense and Infectious Diseases, George Mason University, Manassas, VA 20110, USA
National Institutes of Health, Molecular Virology Section, Laboratory of Molecular Microbiology, NIAID, Bethesda, Maryland 20892, USA
Department of Microbiology, Immunology, and Tropical Medicine, The George Washington University Medical Center, Washington, DC 20037, USA


© Easley et al; licensee BioMed Central Ltd. 2011

This article is published under license to 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.