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Journal of Virology, September 2009, p. 8470-8481, Vol. 83, No. 17
0022-538X/09/$08.00+0     doi:10.1128/JVI.02568-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Analysis of Human Immunodeficiency Virus Type 1 Viremia and Provirus in Resting CD4+ T Cells Reveals a Novel Source of Residual Viremia in Patients on Antiretroviral Therapy {triangledown} ,{dagger}

Timothy P. Brennan,1 John O. Woods,2 Ahmad R. Sedaghat,3 Janet D. Siliciano,3 Robert F. Siliciano,3,4 and Claus O. Wilke2,5*

Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205,1 Institute for Cell and Molecular Biology, The University of Texas at Austin, Austin, Texas 78712,2 Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205,3 Howard Hughes Medical Institute, Baltimore, Maryland 21205,4 Center for Computational Biology and Bioinformatics and Section of Integrative Biology, The University of Texas at Austin, Austin, Texas 787125

Received 12 December 2008/ Accepted 27 May 2009

Highly active antiretroviral therapy (HAART) can reduce human immunodeficiency virus type 1 (HIV-1) viremia to clinically undetectable levels. Despite this dramatic reduction, some virus is present in the blood. In addition, a long-lived latent reservoir for HIV-1 exists in resting memory CD4+ T cells. This reservoir is believed to be a source of the residual viremia and is the focus of eradication efforts. Here, we use two measures of population structure—analysis of molecular variance and the Slatkin-Maddison test—to demonstrate that the residual viremia is genetically distinct from proviruses in resting CD4+ T cells but that proviruses in resting and activated CD4+ T cells belong to a single population. Residual viremia is genetically distinct from proviruses in activated CD4+ T cells, monocytes, and unfractionated peripheral blood mononuclear cells. The finding that some of the residual viremia in patients on HAART stems from an unidentified cellular source other than CD4+ T cells has implications for eradication efforts.

* Corresponding author. Mailing address: Section of Integrative Biology, University of Texas at Austin, 1 University Station C0930, Austin, TX 78712. Phone: (512) 471-6028. Fax: (512) 471-3878. E-mail: cwilke{at}mail.utexas.edu

{triangledown} Published ahead of print on 17 June 2009.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, September 2009, p. 8470-8481, Vol. 83, No. 17
0022-538X/09/$08.00+0     doi:10.1128/JVI.02568-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Dinoso, J. B., Rabi, S. A., Blankson, J. N., Gama, L., Mankowski, J. L., Siliciano, R. F., Zink, M. C., Clements, J. E. (2009). A Simian Immunodeficiency Virus-Infected Macaque Model To Study Viral Reservoirs That Persist during Highly Active Antiretroviral Therapy. J. Virol. 83: 9247-9257 [Abstract] [Full Text]  


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