Dr. Wen-Zhe Ho and others from The Childrens Hospital of Philadelphia report, in the January 1st issue of the Journal of Infectious Diseases, that methadone “significantly enhanced” HIV infection when added to cultured human fetal microglia and blood monocyte-derived macrophages.
Methadone up-regulates expression of CCR5, “a primary coreceptor for macrophage-tropic HIV entry into macrophages,” they say. Recent data showing that morphine induces CCR5 gene expression in human T lymphoid cells supports this as a possible mechanism whereby methadone potentiates HIV infection, the authors note.
“Most importantly, the addition of methadone to the cultures of latently infected peripheral blood mononuclear cells [PBMC] from HIV-infected patients enhanced viral activation and replication,” they report.
Methadones effects on the HIV long-terminal repeat (LTR) promoter “may be the basis for methadone-induced activation of HIV in latently infected PBMC,” Dr. Ho and colleagues add. Their experiments suggest that methadone may inhibit endogenous beta-chemokine production by monocyte-derived macrophages and activate HIV LTR.
Given the prevalence of HIV in the methadone-treatment population, “it is essential to understand the immunologic consequences of methadone treatment and its role in the immunopathogenesis of HIV disease,” Dr. Hos team concludes.