AIDSWEEKLY Plus, Monday, 10 March 1997
Daniel J. DeNoon, Senior Editor
The cytokines interleukin 13 (IL-13) and tumor necrosis factor alpha (TNF-(alpha)) synergistically inhibit HIV infection of macrophages.
The in vitro findings suggest that IL-13 may represent a novel immunotherapy for patients with HIV infection, in whom high levels of TNF-(alpha) occur.
Robert T. Bailer and colleagues of the Wistar Institute, Philadelphia, Pennsylvania, examined the effects of IL-13 both alone and in combination with TNF-(alpha) in cultures of primary human macrophages infected with the HIV-1 strain 89.6.
Bailer reported the study findings at the Fourth Conference on Retroviruses and Opportunistic Infections, held January 22-26 in Washington, D.C.
"These results suggest TNF-(alpha) may act to control viral infection within specific microenvironments where IL-13 is expressed, and implies a 'combined' antiviral effect in vivo after immunotherapeutic administration of IL-13 to HIV-1 patients," Bailer et al. wrote in their presentation abstract.
When both IL-13 and TNF-(alpha) were present in macrophage cultures, TNF-(alpha) apparently decreased the infectivity of HIV infected cells while IL-13 reduced viral expression.
The two cytokines together had different effects than either cytokine by itself. Cultures treated with both cytokines were eight times less infectious than cultures treated with IL-13 alone. And while TNF-(alpha) alone downregulates CD4, this effect did not occur in the presence of both TNF-(alpha) and IL-13.
"Overall, these results illustrate the potential for synergistic inhibitory effects by IL-13 and TNF-(alpha) in macrophages by their combined effects of reducing HIV-1 infection efficiency without inducing HIV-1 expression from infected macrophages," Bailer et al. wrote.
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