مؤتمر
HIV-1 reactivation after an oxidative stress
| العنوان: | HIV-1 reactivation after an oxidative stress |
|---|---|
| المؤلفون: | Legrand, Sylvie, Vaira, Dolorès, Rentier, Bernard, Piette, Jacques |
| المصدر: | LinkVIII International Conference on AIDS/III STD World Congress, Amsterdam, the Netherlands 19-24 July 1992 (1992); VIIIth International Conference on AIDS, Amsterdam, Netherlands [NL], 1992 Jul 19-24 |
| بيانات النشر: | CONGREX Holland B.V., 1992. |
| سنة النشر: | 1992 |
| مصطلحات موضوعية: | 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, Human health sciences, Immunology & infectious disease, Sciences de la santé humaine, Immunologie & maladie infectieuse |
| الوصف: | 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. |
| نوع الوثيقة: | conference paper http://purl.org/coar/resource_type/c_5794Test conferenceObject |
| اللغة: | English |
| الوصول الحر: | https://orbi.uliege.be/handle/2268/7967Test |
| رقم الانضمام: | edsorb.7967 |
| قاعدة البيانات: | ORBi |
| الوصف غير متاح. |