Naltrexone, a drug used in the treatment of heroin addiction and alcoholism, may increase the effectiveness of the antiretroviral drugs zidovudine (AZT) and indinavir, which are used in the treatment of human immunodeficiency virus (HIV). Naltrexone blocks opioid receptors in the brain preventing the “high” associated with the use of heroin and other opioids. Although the mechanism of the synergistic activity of naltrexone, AZT, and indinavir is unknown, the interaction of naltrexone with opioid receptors may play a role.
Researchers at the Institute for Brain and Immune Disorders, Minneapolis Medical Research Foundation, Hennepin County Medical Center, and the University of Minnesota Medical School in Minneapolis conducted an in vitro study with CD4+ T lymphocytes. These cells express opioid receptors and are the primary cells targeted by HIV.
Cells were obtained from the blood of HIV-1-seronegative individuals and then infected with HIV-1. Cells were incubated for 4 days with AZT, indinavir, naltrexone or combinations of the drugs. HIV-1 p24 antigen levels were measured using an enzyme-linked immunoassay. The researchers found that naltrexone alone had no effect on HIV-1 expression by the cells, but when the drug was added to cell cultures containing AZT or indinavir, the antiviral activity of these drugs increased.
WHAT IT MEANS: Naltrexone is a novel approach to HIV treatment since it appears to target the cells infected with the virus rather than the virus itself, unlike current treatment medications.
The NIDA-funded study, led by Dr. Phillip Peterson, appears in the November 2001 issue of Drug and Alcohol Dependence.
The above post is reprinted from materials provided by NIH/National Institute On Drug Abuse. Note: Content may be edited for style and length.
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