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Journal of Virology, February 2002, p. 1673-1681, Vol. 76, No. 4
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.76.4.1673-1681.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Department of Microbiology, Immunology and Molecular Genetics,1 Department of Medicine,2 AIDS Institute, School of Medicine, University of California at Los Angeles, Los Angeles, California 900953
Received 18 September 2001/ Accepted 13 November 2001
Highly active antiretroviral therapy has succeeded in many cases in suppressing virus production in patients infected with human immunodeficiency virus (HIV); however, once treatment is discontinued, virus replication is rekindled. One reservoir capable of harboring HIV in a latent state and igniting renewed infection once therapy is terminated is a resting T cell. Due to the sparsity of T cells latently infected with HIV in vivo, it has been difficult to study viral and cellular interactions during latency. The SCID-hu (Thy/Liv) mouse model of HIV latency, however, provides high percentages of latently infected cells, allowing a detailed analysis of phenotype. Herein we show that latently infected cells appear phenotypically normal. Following cellular stimulation, the virus completes its life cycle and induces phenotypic changes, such as CD4 and major histocompatibility complex class I down-regulation, in the infected cell. In addition, HIV expression following activation did not correlate with expression of the cellular activation marker CD25. The apparently normal phenotype and lack of HIV expression in latently infected cells could prevent recognition by the immune response and contribute to the long-lived nature of this reservoir.
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