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HIV-1 reactivation after an oxidative stress
Legrand, Sylvie; Vaira, Dolorès; Rentier, Bernard et al.
1992In LinkVIII International Conference on AIDS/III STD World Congress, Amsterdam, the Netherlands 19-24 July 1992


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Keywords :
EGIS, HIV Long Terminal Repeat, HIV-1, Oxidative Stress, RNA-Directed DNA Polymerase, Hela Cells, Cell Line, Trans-Activation (Genetics), Hydrogen Peroxide, Anti-HIV Agents, T-Lymphocytes, Oxidation-Reduction, Human, Cats, Animal, In Vitro, genetics, ICA8
Abstract :
[en] OBJECTIVES: A common denominator shared by several HIV-1 reactivation agents such as certain cytokines, UV irradiation and heat shock is their ability to cause stress response. Consequently, we have investigated the effects of oxidative stress on HIV-1 reactivation, knowing that HIV-1 latently infected T cells can be exposed in vivo to such a stress when blood phagocytes are stimulated during inflammatory reactions. METHODS: The promonocytic (U1) and lymphocytic (ACH-2) cell lines, both HIV-1 chronically infected, were used to study the reactivation phenomenon. To test wether HIV-1 reactivation is mediated by LTR transactivation, the HeLa HIV-1 CAT cell line, which carries an integrated DNA cartridge containing CAT gene under control of HIV-1 LTR, was also exposed to an oxidative stress. RESULTS: Hydrogen peroxide exposure of U1 cells leads to an increased reverse transcriptase (RT) activity in supernatant fluid. Over the optimal concentrations range (0.5 to 1 mM), a four to fivefold stimulation level is reached. Below these concentrations, stress conditions are not sufficient and above, they induce a too important lethal effect. Immunofluorescence carried out on stressed U1 cells shows that H2O2 leads to HIV-1 gene expression activation and not to a release of viral particles from damaged cells. H2O2 also induces a stimulation of CAT activity in HeLa HIV-1 CAT cells. Intracellular singulet oxygen (1O2) is also able to induce an increase of RT activity in supernatant fluid of U1 and ACH-2 cells and a stimulation of CAT activity in HeLa HIV-1 CAT cells. A dose-response curve can also be demonstrated. In order to transpose these in vitro experiments to situations encountered in vivo, activated phagocytes were cocultivated with HeLa HIV-1 CAT cells. A weak stimulation of CAT activity was detected. CONCLUSIONS: Cellular oxidative damages induce HIV-1 LTR transactivation leading to viral gene expression and consequently to a burst of virus production. DNA damages induced by oxidative stress could be at the onset of HIV-1 reactivation. Experiments are now in progress to elucidate the mechanisms leading to HIV-1 reactivation after an oxidative stress.
Disciplines :
Immunology & infectious disease
Author, co-author :
Legrand, Sylvie ;  Université de Liège - ULiège > Virologie - Immunologie
Vaira, Dolorès ;  Centre Hospitalier Universitaire de Liège - CHU > Immuno-hématologie
Rentier, Bernard  ;  Université de Liège - ULiège > Département de Microbiologie > Virologie fondamentale et Immunologie
Piette, Jacques ;  Université de Liège - ULiège > Département des sciences de la vie > Virologie - Immunologie
Language :
Title :
HIV-1 reactivation after an oxidative stress
Publication date :
Event name :
VIIIth International Conference on AIDS
Event place :
Amsterdam, Netherlands
Event date :
1992 Jul 19-24
Audience :
Main work title :
LinkVIII International Conference on AIDS/III STD World Congress, Amsterdam, the Netherlands 19-24 July 1992
Publisher :
CONGREX Holland B.V., Amsterdam, Netherlands
Funders :
Harvard University [US-MA] [US-MA]
Dutch Foundation AIDS Conference 1992
International AIDS Society
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