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Papers In Press, published online ahead of print July 16, 2004
Research Center in Infectious Diseases, RC709, CHUL Research Center, Quebec, Quebec G1V 4G2
Corresponding Author: michel.j.tremblay{at}crchul.ulaval.ca
A chronic state of immune hyperactivation is a feature of human immunodeficiency virus type-1 (HIV-1) infection. Studies on the molecular mechanisms by which HIV-1 can modulate the activation state of T cells indicate that both Nef and Tat can alter T cell activation. However, the vast majority of data has been obtained from experiments performed with vectors encoding a single virus protein. We demonstrate that infection of human CD4+ T lymphocytes with fully infectious HIV-1 leads to a hyper-responsiveness of the IL-2 promoter. Hypersensitivity in HIV-1-infected T cells was observed upon stimulation with various agents that are engaging different signal transduction pathways. Experiments performed with recombinant HSA-encoding HIV-1 indicated that the virus-infected cells are the cells with an enhanced response. Both Nef and Tat are involved in this virus-mediated enhancing effect on IL-2 promoter activity. Interestingly, whereas Nef seems to be acting mainly through hyperactivation of NFAT, Tat acts in an NFAT-independent manner. Mobility shift experiments demonstrated that the HIV-1-associated priming of human T cells for stimulation results in a greater induction of transcription factors recognized as essential players in T cell activation, i.e. NFAT, NF-
J. Biol. Chem, 10.1074/jbc.M407477200
Submitted on July 6, 2004
Revised on July 16, 2004
Accepted on July 16, 2004
Hyper-responsiveness to stimulation of human immunodeficiency virus-infected CD4+ T cells requires Nef and Tat virus gene products and results from higher NFAT, NF-
B, and AP-1 induction
B, and AP-1. A hyperresponsive state was also established upon HIV-1 infection of a more natural cellular reservoir, i.e. primary CD4+ T lymphocytes. Considering that the HIV-1 life cycle is tightly regulated by the T cell signaling machinery, the priming for activation of a major viral reservoir represents a means by which this retrovirus can create an ideal cellular microenvironment for its propagation and maintenance.
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