Abstract |
Interleukin (IL)-18 is an interferon ( IFN)-gamma-inducing factor and contributes to the Th1 immune response. IL-18 added after infection of peripheral blood mononuclear cells (PBMC) with monocyte-tropic human immunodeficiency virus type 1 (HIV-1) inhibited p24 antigen production by a maximum of 72%. IFN-gamma levels in these cultures were increased, and a significant inverse relationship between HIV-1 production and IFN-gamma levels was observed. A neutralizing anti-IFN-gamma antibody reversed the IL-18 inhibitory effect. Preincubation of PBMC with IL-18 before infection inhibited p24 without additional IL-18 (64%). However, compared with the degree of IL-18 inhibition observed after a 4-day culture, no additional IL-18 inhibitory effect was observed during days 5-13. IL-18 also reduced cell surface expression of the HIV-1 receptor CD4. These results demonstrate that IL-18 inhibited HIV-1 production in PBMC through intermediate IFN-gamma. Furthermore, inhibition was present during the early stages of viral infection and was associated with reduced HIV-1 receptor expression.
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Authors | H J Choi, C A Dinarello, L Shapiro |
Journal | The Journal of infectious diseases
(J Infect Dis)
Vol. 184
Issue 5
Pg. 560-8
(Sep 01 2001)
ISSN: 0022-1899 [Print] United States |
PMID | 11494162
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- CD4 Antigens
- HIV Core Protein p24
- Interleukin-18
- Interferon-gamma
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Topics |
- CD4 Antigens
(metabolism)
- Cells, Cultured
- HIV Core Protein p24
(metabolism)
- HIV Infections
(virology)
- HIV-1
(drug effects, physiology)
- Humans
- Interferon-gamma
(biosynthesis)
- Interleukin-18
(pharmacology)
- Leukocytes, Mononuclear
(virology)
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