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Journal of Virology, February 1999, p. 1447-1452, Vol. 73, No. 2
Université Pierre et Marie
Curie,1 and
URA 1679 et UPR 42 CNRS,
Ecole Normale Supérieure,2 Paris, France
Received 16 June 1998/Accepted 12 November 1998
In the course of our studies on oxidative stress as a component of
pathological processes in humans, we showed that microintrusion into
cells with microcapillary and ultramicroelectrochemical detection could mimic many types of mechanical intrusion leading to an
instant (0.1 s) and high (some femtomoles) burst release of
H2O2. Specific inhibitors of NADPH enzymes seem
to support the assumption that this enzyme is one of the main targets
of our experiments. Also, human immunodeficiency virus type 1 (HIV-1)
gp160 inhibits the cooperative response of uninfected T cells as well
as Tat protein release by infected cells does. In this study, we
analyzed in real time, lymphocyte per lymphocyte, the T-cell response
following activation in relation to the redox state. We showed that the immunosuppressive effects of HIV-1 Tat and gp160 proteins and oxidative
stress are correlated, since the native but not the inactivated Tat and
gp160 proteins inhibit the cellular immune response and enhance
oxidative stress. These results are consistent with a role of the
membrane NADPH oxidase in the cellular response to immune activation.
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Amplification of the Inflammatory Cellular Redox State by Human
Immunodeficiency Virus Type 1-Immunosuppressive Tat and gp160
Proteins
*
Corresponding author. Mailing address: UPR42 CNRS,
Département de Chimie, Ecole Normale Supérieure,
75005 Paris, France. Phone: 33-1-44323641. Fax: 33-1-44323325. E-mail: Monique.Vuillaume{at}ens.fr.
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