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Journal of Virology, January 1999, p. 290-296, Vol. 73, No. 1
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

RNase L Inhibitor Is Induced during Human Immunodeficiency Virus Type 1 Infection and Down Regulates the 2-5A/RNase L Pathway in Human T Cells

Camille Martinand, Céline Montavon,dagger Tamim Salehzada, Michelle Silhol, Bernard Lebleu, and Catherine Bisbal*

Institut de Génétique Moléculaire de Montpellier (UMR 5535, CNRS-Université de Montpellier II), 34293 Montpellier Cedex 5, France

Received 26 June 1998/Accepted 22 September 1998

The interferon-regulated 2-5A/RNase L pathway plays a major role in the antiviral and antiproliferative activities of these cytokines. Several viruses, however, have evolved strategies to escape the antiviral activity of the 2-5A/RNase L pathway. In this context, we have cloned a cDNA coding for the RNase L inhibitor (RLI), a protein that specifically inhibits RNase L and whose regulated expression in picornavirus-infected cells down regulates the activity of the 2-5A/RNase L pathway. We show here that RLI increases during the course of human immunodeficiency virus type 1 (HIV-1) infection, which may be related to the downregulation of RNase L activity that has been described to occur in HIV-infected cells. In order to establish a possible causal relationship between these observations, we have stably transfected H9 cells with RLI sense or antisense cDNA-expressing vectors. The overexpression of RLI causes a decrease in RNase L activity and a twofold enhancement of HIV production. This increase in HIV replication correlates with an increase in HIV RNA and proteins. In contrast, reduction of RLI levels in RLI antisense cDNA-expressing clones reverses the inhibition of RNase L activity associated with HIV multiplication and leads to a threefold decrease in the viral load. This anti-HIV activity correlated with a decrease in HIV RNA and proteins. These findings demonstrate that the level of RLI, via its modulation of RNase L activity, can severely impair HIV replication and suggest the involvement of RLI in the inhibition of the 2-5A/RNase L system observed during HIV infection.

* Corresponding author. Mailing address: Institut de Genetique Moleculaire de Montpellier, UMR 5535, CNRS-Université de Montpellier II, 1919, route de Mende, 34293 Montpellier Cedex 5, France. Phone: 33-4-67-61-36-58. Fax: 33-4-67-04-02-45. E-mail: bisbal{at}jones.igm.cnrs-mop.fr.

dagger Present address: Laboratoire Retrovirus, ORSTOM, 34032 Montpellier Cedex 1, France.

Journal of Virology, January 1999, p. 290-296, Vol. 73, No. 1
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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