Assessment of in Vitro Cytikine Response to Human Immunodeficiency Virus Antigens

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Addis Abeba Universty


The study of mononuclear cell responses after human immunodeficiency virus type-l (HIV-l ) activation may help in providing some insight into the understanding of the pathogenic mechanisms of HIV infection or acquired immunodeficiency syndrome (AIDS)-related disorders. The secretion of three cytokines, interleukin-6 (IL-6) , tumor necrosis factor (TNF)-alpha, and interferon(IFN)-gamma by peripheral blood mononuclear cells(PBMC) was determined after in vitro stimulation with heat -inactivated HIV-I antigens, using cytokine-specific monoclonal antibodies and an indirect immunofluorescence technique. HIV-l antigen stimulation of PBMC from healthy donors did not induce the intracellular accumulation of IL-6, TNF-alpha, or IFN-gamma. Similarly, cells from asymptomatic HIV-infected subjects did not result in cytokine production either spontaneously or f ollowing stimulation with HIV antigen. After activation with mitogen o r antigen,cells from HIV-infected persons produced amounts of IL-6, TNF-alpha and IFN-gamma comparable to that of cells from healthy individuals. Furthermore, co-st imulation o f normal PBMC with HIVantigen plus L.donovani resulted in intracellular accumulation of IL-6 and TNF-alpha comparab~ e to that of cells that were activated with Leishmania antigen alone. Heat-inactivated HIV-l antigen does n o t appear to induce or modulate cytokine production by PBMC. A defect in cytokine production is also accompanied by i nh ibition of PPD-induced lymphoproliferative responses . Elevated levels o f serum cytokines have been demonstrated in patients with HIV infection indicating their role in the pathogenesis of HIV-associated infections. Theref ore, data from our results may partly support the idea that t he cause o f the abnormal l y increased cycokine levels in t he sera o f HIV-infected subjects x might be jue to a variety of opportunistic pathogens that these patients contract. As cytokines have been shown t o up-regulate HIV repl ication, our data addit i onally demonstrate a role f o r opportunistic infections in cytokine induced transactivation of HIV-l and disease progression.



Assessment of in Vitro Cytikine Response