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Journal of Virology, February 2007, p. 1660-1670, Vol. 81, No. 4
0022-538X/07/$08.00+0     doi:10.1128/JVI.01396-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Novel Pathway for Induction of Latent Virus from Resting CD4+ T Cells in the Simian Immunodeficiency Virus/Macaque Model of Human Immunodeficiency Virus Type 1 Latency{triangledown}

Anding Shen,1* Hung-Chih Yang,1 Yan Zhou,1 Amanda J. Chase,1 Jean D. Boyer,2 Hao Zhang,3 Joseph B. Margolick,3 M. Christine Zink,4 Janice E. Clements,4 and Robert F. Siliciano1,5

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland,1 Department of Pathology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania,2 Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland,3 Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland,4 Howard Hughes Medical Institute, Baltimore, Maryland5

Received 3 July 2006/ Accepted 7 November 2006

Although combination therapy allows the suppression of human immunodeficiency virus type 1 (HIV-1) viremia to undetectable levels, eradication has not been achieved because the virus persists in cellular reservoirs, particularly the latent reservoir in resting CD4+ T lymphocytes. We previously established a simian immunodeficiency virus (SIV)/macaque model to study latency. We describe here a novel mechanism for the induction of SIV from latently infected resting CD4+ T cells. Several human cell lines including CEMx174 and Epstein-Barr virus-transformed human B-lymphoblastoid cell lines mediated contact-dependent activation of resting macaque T cells and induction of latent SIV. Antibody-blocking assays showed that interactions between the costimulatory molecule CD2 and its ligand CD58 were involved, whereas soluble factors and interactions between T-cell receptors and major histocompatibility complex class II were not. Combinations of specific antibodies to CD2 also induced T-cell activation and virus induction in human resting CD4+ T cells carrying latent HIV-1. This is the first demonstration that costimulatory signals can induce latent virus without the coengagement of the T-cell receptor, and this study might provide insights into potential pathways to target latent HIV-1.

* Corresponding author. Present address: Department of Biology, Calvin College, 1726 Knollcrest Circle SE, Grand Rapids, MI 49546. Phone: (616) 526-6025. Fax: (616) 526-6501. E-mail: as28{at}calvin.edu.

{triangledown} Published ahead of print on 6 December 2006.

Journal of Virology, February 2007, p. 1660-1670, Vol. 81, No. 4
0022-538X/07/$08.00+0     doi:10.1128/JVI.01396-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Marini, A., Harper, J. M., Romerio, F. (2008). An In Vitro System to Model the Establishment and Reactivation of HIV-1 Latency. J. Immunol. 181: 7713-7720 [Abstract] [Full Text]  


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