Amplification of the inflammatory cellular redox state by human immunodeficiency virus type 1-immunosuppressive tat and gp160 proteins.

Abstract:

: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.

journal_name

J Virol

journal_title

Journal of virology

authors

Lachgar A,Sojic N,Arbault S,Bruce D,Sarasin A,Amatore C,Bizzini B,Zagury D,Vuillaume M

doi

10.1128/JVI.73.2.1447-1452.1999

subject

Has Abstract

pub_date

1999-02-01 00:00:00

pages

1447-52

issue

2

eissn

0022-538X

issn

1098-5514

journal_volume

73

pub_type

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