alled "inductive" cytokines, such as tumor necrosis factor-alpha (TNF-alpha), interleukin 1-beta (IL-1 beta), and interleukin-6 (IL-6), can markedly reduce viral replication. Conversely, as LIR scientists first described in 1987, even resting, latently infected cells can be induced to actively produce HIV when cytokines such as TNF-alpha are added. More recent LIR experiments have shown that other stimuli, such as the activation of immune system cells by immunization, can also induce latently infected cells to actively produce HIV. In addition to these factors, a group of molecules called CC-chemokines, which suppress the replication of certain strains of HIV, can enhance the replication of HIV in some circumstances.

"HIV disease is a multifactorial process controlled by the complicated interplay of stimulatory and inhibitory factors concentrated in the lymphoid tissue, the centers of immune activity in the body," Dr. Fauci notes.

At the Chicago symposium, Dr. Fauci will present data from in vitro experiments involving latently infected CD4+ T cells drawn from HIV-infected, HAART-treated individuals, as well as from HIV-infected patients not receiving HAART.

In one series of experiments, the researchers found that after adding HAART to cultures of latently infected, resting CD4+ T cells, they were unable to induce with cytokines the production of HIV from the cells of either group of patients.

"However, when we took HAART out of the cultures, we were able to rapidly induce HIV replication with cytokines, even in cells from patients who had been on HAART for many months," says Dr. Fauci.

In another in vitro experiment, the researchers sought to determine if they coul
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Contact: Greg Folkers
gfolkers@nih.gov
301-496-2263
NIH/National Institute of Allergy and Infectious Diseases
2-Feb-1998

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