Comparison of a PCR-based assay and the MT2 coculture method for the follow-up of syncytium inducing strains in HIV patients under antiprotease therapy

Conference (1998)

Prévalence du virus de l'hépatite G dans une population d'hémodialysés chroniques

Conference (1997)

HIV-1 promoter activation following an oxidative stress mediated by singlet oxygen

in Journal of Photochemistry & Photobiology B : Biology (1993), 17(3), 229-237

Various biological processes, such as photosensitization or inflammatory reactions, can generate singlet oxygen (O-1(2)) as one of the major oxidative species. Because this oxidant can be generated either ... [more ▼]

Various biological processes, such as photosensitization or inflammatory reactions, can generate singlet oxygen (O-1(2)) as one of the major oxidative species. Because this oxidant can be generated either extracellularly or intracellularly, it can cause severe damage to various biological macromolecules, even to those deeply embedded inside the cells such as DNA. Sublethal biological modifications induced by different DNA-damaging agents can promote various cellular responses initiated by the activation of various cellular genes and certain heterologous viruses. Since O-1(2) fulfils essential prerequisites for a genotoxic substance, we have examined the effects of an oxidative stress, mediated by this species, on cells harbouring a heterologous promoter-leader sequence derived from the human immunodeficiency virus type 1 (HIV-1). Our results demonstrate that HIV-1 long terminal repeat (LTR), integrated into the cellular I)NA of epithelial cells, can be transactivated following an oxidative stress mediated by O-1(2). In addition, using HIV-1 latently infected promonocytes or lymphocytes, it can be shown that virus reactivation can be induced through a sublethal dose of O-1(2) generated intracellularly. An extracellular generation of O-1(2) can promote a substantial lethal effect without HIV-1 reactivation. These data may be relevant to the understanding of the events converting a latent infection into a productive one and to the appearance of the acquired immune deficiency syndrome. [less ▲]

HIV-1 reactivation after an oxidative stress

in LinkVIII International Conference on AIDS/III STD World Congress, Amsterdam, the Netherlands 19-24 July 1992 (1992)

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 ... [more ▼]

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. [less ▲]

Activation of human immunodeficiency virus type 1 by an oxidative stress

in AIDS Research and Human Retroviruses (1990)

Diagnosis by PCR of HIV-1 infection in seronegative individuals at risk

in AIDS Research and Human Retroviruses (1990), 6(2), 173-174

Diagnosis of HIV-1 in African couples : comparison of serology and PCR

in Cinquième conférence internationale sur le SIDA : le défi scientifique et social (1989)

OBJECTIVE: Search for the rate of HIV-1 contamination among seronegative sexual partners of seropositive individuals. METHODS: Classical serological methods (EIA, WB) and PCR. SERIES: 36 heterosexual ... [more ▼]

OBJECTIVE: Search for the rate of HIV-1 contamination among seronegative sexual partners of seropositive individuals. METHODS: Classical serological methods (EIA, WB) and PCR. SERIES: 36 heterosexual couples from central Africa, accounting for a total of 73 persons: 13/37 seropositive women, 23/36 seropositive men. All couples were serologically discordant, i.e. one partner was seropositive. CONCLUSIONS: In such a population, particularly at risk of HIV contamination, the rate of false negative serological diagnosis reached 70%. [less ▲]

In vivo model of varicella-zoster virus latency in the nervous system

Conference (1989)

Natural infection of Swiss mice by the Mouse Mammary Tumor Virus (MMTV). 2. Studies on the pathway of infection

in Archives Internationales de Physiologie, de Biochimie et de Biophysique (1984), 92(1), 28