Browsing by Author "Dawit Welday"

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    Assessment of in Vitro Cytikine Response to Human Immunodeficiency Virus Antigens.
    (Addis Abeba Universty, 1992-12) Dawit Welday; Audrey Hathaway
    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 following stimulation with HIV antigen. After activation with mitogen orantigen, 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 of normal PBMC with HIV antigenplus L.donovani resulted in intracellular accumulation of IL-6 and TNF-alpha comparable to that of cells that were activated with Leishmania antigen alone. Heat-inactivated HIV-lantigen doe’s n o t appear to induce or modulate cytokine production by PBMC. A defect in cytokine production is also accompanied by inhibition of PPD-inducedly mph proliferative responses. Elevated levels of serum cytokines have been demonstrated in patients with HIV infection indicating their role in the pathogenesis of HIV-associated infections. There f ore, data from our results may partly support the idea that the cause of the abnormal ly increased cycokine levels in the sera of HIV-infected subject might bejue to a variety of opportunistic pathogens that these patients contract. As cytokines have been shown to up-regulate HIV replication, our data additionally demonstrate a role for opportunistic infections in cytokine induced transactivation of HIV-l and disease progression.