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Morphine enhances HIV infection of neonatal macrophages
Yuan Li1, Jeffrey D Merrill, Kathy Mooney
1Division of Immunologic and Infectious Diseases, The Children's Hospital of Philadelphia, 34th Street & Civic Center Boulevard, Philadelphia, PA 19104, U.S.A.
Abstract:
Perinatal transmission of HIV accounts for almost all new HIV infections in children. There is an increased risk of perinatal transmission of HIV with maternal illicit substance abuse. Little is known about neonatal immune system alteration and subsequent susceptibility to HIV infection after morphine exposure. We investigated the effects of morphine on HIV infection of neonatal monocyte-derived macrophages (MDM). Morphine significantly enhanced HIV infection of neonatal MDM. Morphine-induced HIV replication in neonatal MDM was completely suppressed by naltrexone, the opioid receptor antagonist. Morphine significantly up-regulated CCR5 receptor expression and inhibited the endogenous production of macrophage inflammatory protein-1beta in neonatal MDM. Thus, morphine, most likely through alteration of beta-chemokines and CCR5 receptor expression, enhances the susceptibility of neonatal MDM to HIV infection, and may have a cofactor role in perinatal HIV transmission and infection.
Insights
Maternal morphine use increases infant HIV infection risk by enhancing viral replication in neonatal immune cells. Naltrexone, an opioid antagonist, fully blocked this effect, suggesting a target for intervention.
Area of Science:
- Immunology
- Virology
- Neonatal Health
Background:
- Perinatal HIV transmission is a major cause of pediatric HIV infections.
- Maternal substance abuse, including morphine, is linked to increased perinatal HIV transmission risk.
- The impact of neonatal morphine exposure on immune cells and HIV susceptibility is not well understood.
Purpose of the Study:
- To investigate the effects of morphine on HIV infection in neonatal monocyte-derived macrophages (MDM).
- To explore the mechanisms by which morphine influences HIV susceptibility in the neonatal immune system.
Main Methods:
- Neonatal MDM were exposed to morphine.
- HIV infection levels in MDM were measured.
- CCR5 receptor expression and beta-chemokine production (macrophage inflammatory protein-1beta) were analyzed.
- The effect of naltrexone, an opioid receptor antagonist, was evaluated.
Main Results:
- Morphine significantly enhanced HIV infection and replication in neonatal MDM.
- Morphine exposure led to increased CCR5 receptor expression on neonatal MDM.
- Morphine inhibited the endogenous production of macrophage inflammatory protein-1beta.
- Naltrexone completely suppressed morphine-induced HIV replication in neonatal MDM.
Conclusions:
- Morphine enhances neonatal susceptibility to HIV infection, likely by altering beta-chemokines and CCR5 receptor expression.
- Morphine may play a cofactor role in perinatal HIV transmission and infection.
- Targeting opioid receptors with antagonists like naltrexone could be a strategy to mitigate HIV risk in neonates exposed to morphine.