a study to evaluate the ability of tnfr:fc to decrease the amount of il-6 (interleukin-6) and tnf-alpha (tumor necrosis factor) in hiv-infected patients

Conditions: HIV Infections

Summary: the purpose of this study is to determine if tnfr:fc (a molecule that attaches to tnf) can lower the amount of il-6 in hiv-positive patients. this study will also examine the effect of tnfr:fc on tnf-alpha. il-6 and tnf-alpha are 2 substances produced by the immune system that may increase the rate of hiv replication. il-6 and tnf-alpha are produced naturally by the body. high levels of tnf-alpha lead to increased il-6 production and increased hiv replication, therefore helping the virus infect the body. hiv-positive patients who receive il-2 (interleukin-2, a protein that helps the immune system fight infection) tend to have higher levels of il-6 and tnf-alpha than patients not receiving il-2. these increased levels may contribute to some of the flu-like symptoms related to il-2 administration. tnfr:fc can neutralize tnf-alpha to decrease the action of tnf-alpha and, in turn, decrease the amount of il-6 in the body. tnfr:fc may, therefore, have a role in the treatment of hiv disease or in relieving some of the symptoms related to il-2 administration.

both interleukin-6 (il-6) and tumor necrosis factor-alpha (tnf-alpha) are substances naturally produced by the body's immune system. evidence suggests that tnf-alpha production may be excessive or inappropriate in hiv-infected patients. elevated tnf-alpha levels can result in increased il-6 production and possibly increased hiv replication. tnfr:fc is a modification of a natural substance that binds to tnf-alpha and neutralizes its activity. it is postulated that tnfr:fc may result in decreased activity of tnf-alpha and lower il-6 levels. hiv-infected patients who receive interleukin-2 (il-2) have been shown to have higher tnf-alpha and il-6 levels than those who do not receive il-2. it is thought that these higher levels of tnf-alpha and il-6 may contribute to some of the flu-like symptoms experienced by patients receiving il-2. by decreasing the amount of il-6 in the body and by decreasing the action of tnf-alpha in the body, tnfr:fc may have a role in the treatment of hiv disease or in alleviating some of the symptoms related to il-2 administration. six patients from each of the 3 treatment arms of actg 328 (haart alone, haart plus intravenous (iv) rhil-2, and haart plus subcutaneous (sc) rhil-2) who are about to be randomized to step ii of actg 328 may participate in this prospective, nested substudy. patients randomized to the interleukin-2 (il-2) arms of actg 328 are pretreated with tnfr:fc (administered by infusion over 30 minutes) at week 16 of actg 928 (course 3, week 28 of actg 328), just prior to initiation of il-2. those randomized to the highly active antiretroviral therapy (haart) only arm of actg 328 receive treatment with tnfr:fc at week 16 of actg 928 (week 28 of actg 328).

Eligibility criteria:
inclusion criteria you may be eligible for this study if you: * are hiv-positive. * are enrolled in actg 328. * agree to practice abstinence or use barrier methods of birth control during the study. * are at least 18 years old. exclusion criteria you will not be eligible for this study if you: * have any active opportunistic (hiv-associated) infections. * have any medical condition or psychological issue that would interfere with study requirements. * are pregnant or breast-feeding. * are receiving any experimental drug other than il-2. * are receiving certain other medications.

Keywords: tumor necrosis factor interleukin-2 immunity, cellular antiviral agents interleukin-6 receptors, tumor necrosis factor