UNIVERSITY OF MIAMI
Opiate drug abuse and human immunodeficiency virus (HIV) are two major public health problems. Opiate drug abuse affects many people with substantial adverse impact on society. In the worldwide, more than 40 million people are currently infected with HIV. HIV-associated sensory neuropathy (HIV-SN) is one of the most common neurological complications of HIV infection. The symptoms of HIV-SN are dominated by neuropathic pain. An increased frequency and severity of HIV-induced inflammation in a heroin-abusing population suggests a relationship between HIV infection and opiate abuse. Recent data show that resident immune cells (glia) in the nervous system may represent an important point of intersection between opiate abuse and HIV-SN, and that opiate drugs may accelerate neurodegeneration in HIV-1 infection. Limited attention has so far been devoted to exploring the pathogenesis of interaction of this very painful disorder and opiate abuse. Therefore, there is no effective treatment. The overall goal of this grant is to critically test the hypothesis that activation of glia plays a key role in the interaction of chronic morphine treatment with HIV-SN neuropathic pain. The specific goals of the research proposed here are to (1) to examine the interaction between morphine tolerance and HIV-SN neuropathic pain, and their neurochemical characteristics; and (2) to test the effect of viral vector-mediated production of soluble TNFR (inhibitor of inflammation) on the HIV-pain, morphine tolerance, or the combination of HIV-pain and chronic morphine.