Interleukin-18 enhances HIV-1 production in a human chronically-infected T cell line (H9-V)
✍ Scribed by Agostino Pugliese; Luisa Gennero; Valerio Vidotto; Filippo Speranza; Roberto Tambini; Donato Torre
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 76 KB
- Volume
- 20
- Category
- Article
- ISSN
- 0263-6484
- DOI
- 10.1002/cbf.981
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Interleukin‐18 (IL‐18) is a recently identified immunoregulatory cytokine expressed by activated macrophages, that induces production of interferon‐γ (IFN‐γ) and Th‐1 development. Recently some investigators reported controversial in vitro data on IL‐18 stimulation of HIV‐1 replication in several cell lines. In the present study the effect of IL‐18 on HIV replication in a human chronically HIV‐1‐infected lymphocytic T cell line (H9‐V) was investigated. HIV‐1 replication was determined by an immunoassay method in order to evaluate the content of p24 antigen in the cell culture supernatants. Stimulation of H9‐V cells with IL‐18 resulted in increased production of p24, especially at concentrations of 0.01 μg ml^−1^ and 0.10 μg ml^−1^. Moreover a significant and persistent IL‐18 stimulation of HIV‐1 replication was observed at a concentration of 0.01 μg ml^−1^ during a 7‐day period. Pre‐treatment of IL‐18 with a specific neutralizing monoclonal antibody significantly reduced HIV‐1 replication. These experiments show that IL‐18 promotes the increase of HIV‐1 replication in human chronically‐infected lymphocytic T cells and confirm the role of IL‐18 as a proimflammatory cytokine in stimulating and maintaining HIV‐1 replication during the course of the disease. In a successive set of experiments, since one of the main activities of IL‐18 is the induction of IFN‐γ, we evaluated the effect of this biological modifier on H9‐V cells. In particular, IFN‐γ shows a significant effect on cell replication and on reduction of CD4 and CD71 surface expression. Copyright © 2002 John Wiley & Sons, Ltd.