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Journal of Virology, July 2007, p. 7424-7434, Vol. 81, No. 14
0022-538X/07/$08.00+0     doi:10.1128/JVI.02838-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Primary Cell Model for Activation-Inducible Human Immunodeficiency Virus{triangledown}

Bryan Burke,1 Helen J. Brown,1 Matthew D. Marsden,2 Gregory Bristol,2 Dimitrios N. Vatakis,2 and Jerome A. Zack1,2,3*

Department of Microbiology, Immunology, and Molecular Genetics,1 Department of Medicine, Division of Hematology and Oncology,2 UCLA AIDS Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 900953

Received 21 December 2006/ Accepted 23 April 2007

Quiescent T lymphocytes containing latent human immunodeficiency virus (HIV) provide a long-lived viral reservoir. This reservoir may be the source of active infection that is reinitiated following the cessation of antiretroviral therapy. Therefore, it is important to understand the mechanisms involved in latent infection to develop new strategies to eliminate the latent HIV reservoir. We have previously demonstrated that latently infected quiescent lymphocytes can be generated during thymopoiesis in vivo in the SCID-hu mouse system. However, there is still a pressing need for an in vitro model of HIV latency in primary human cells. Here, we present a novel in vitro model that recapitulates key aspects of dormant HIV infection. Using an enhanced green fluorescent protein-luciferase fusion protein-containing reporter virus, we have generated a stable infection in primary human CD4+ CD8+ thymocytes in the absence of viral gene expression. T-cell activation induces a >200-fold induction of reporter activity. The induced reporter activity originates from a fully reverse-transcribed and integrated genome. We further demonstrate that this model can be useful to study long terminal repeat regulation, as previously characterized NF-{kappa}B response element mutations decrease the activation of viral gene expression. This model can therefore be used to study intricate molecular aspects of activation-inducible HIV infection in primary cells.

* Corresponding author. Mailing address: David Geffen School of Medicine at UCLA, 650 Charles Young Dr. South, Box 951678, 11-934 Factor, Los Angeles, CA 90095-1678. Phone: (310) 825-0876. Fax: (310) 825-6192. E-mail: jzack{at}ucla.edu

{triangledown} Published ahead of print on 2 May 2007.

Journal of Virology, July 2007, p. 7424-7434, Vol. 81, No. 14
0022-538X/07/$08.00+0     doi:10.1128/JVI.02838-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Marsden, M. D., Zack, J. A. (2009). Eradication of HIV: current challenges and new directions. J Antimicrob Chemother 63: 7-10 [Abstract] [Full Text]  


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