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Updated: Jun 25, 2026

Genome-wide RNAi Screening to Identify Host Factors That Modulate Oncolytic Virus Therapy
Published on: April 3, 2018
Enhanced endogenous type I interferon cell-driven survival and inhibition of spontaneous apoptosis by Riluzole
Ammar Achour1, Jean-Pierre M'Bika, Jean-Michel Biquard
1Laboratoire des Interférons/Sarcolectine, Université Paris Descartes, Centre Universitaire des Saint Pères, 45 Rue des Saints-Pères 75006 Paris, France. ammar.achour@biomedicale.univ-paris5.fr
Abstract:
Highly active antiretroviral therapy (HAART), although effective in improving the survival of HIV-1-infected individuals, has not been able to reconstitute the adaptive immune response. We have described the use of novel chemical agents to restore T-cell survival/proliferation by inducing cytokine production. Due to its cationic amphiphilic structure, these molecules appear to enhance immune restoration. In this study, we investigated the action of Riluzole (2-amino-6-trifuromethoxybenzothiazole) in HIV-1 infection. Riluzole is able to increase (effective dose from 1 to 1000 nM) the cell-survival of T cells from HIV-1-infected patients and inhibit spontaneous apoptosis. The immunomodulatory effect of riluzole-sensitized cells was ascribed to endogenous type I interferon (IFN) derived from monocytes. Riluzole might be used for restoring the cell survival of immunocompromised patients and eliminating latent infected cells upon HIV-1 reactivation.
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