1.0 Introduction 
1 . 1 Background 
Infection by the human immunodeficiency virus (HIV) leads to 
progressive depletion of CD4 + T cells which causes an acquired 
immunodeficiency syndrome (AIDS) . Over the past decade, AIDS 
infection has achieved epidemic proportions. Despite 
considerable progress in understanding and diagnosing this 
disease, it has remained refractory to treatment. There are 
currently no effective means to vaccinate susceptible individuals 
or to treat infected patients. Infection by the human 
immunodeficiency virus is typically characterized by an 
asymptomic, or latent, phase of the disease. During this time, 
patients may not exhibit signs of immunodeficiency but 
nonetheless synthesize virus which progressively depletes CD4 + T 
cells and is infectious. It is currently estimated that there 
are over 1 million seropositive cases with latent HIV infection 
in the United States today. These individuals, for whom there 
are no known effective treatments, are likely to progress and 
succumb to this disease. 
For these individuals, a major therapeutic goal is to 
prolong the latent phase of HIV infection. A major interest of 
our laboratory has been to define the molecular basis of HIV gene 
activation in T lymphocytes. We have previously shown that 
activation of HIV gene expression is controlled by a cellular 
transcription factor, NF-/cB (1) . This transcription factor is 
inactive in resting T cells but is stimulated following cell 
activation and induces viral transcription. In addition to NF- 
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Recombinant DNA Research, Volume 18 
