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Inhibition of HIV-1 replication with stable RNAi-mediated knockdown of autophagy factors

By J.J.M. (Julia J. M.) Eekels, S. (Sophie) Sagnier, D. (Dirk) Geerts, R.E. (Rienk) Jeeninga, M. (Martine) Biard-Piechaczyk and B. (Ben) Berkhout

Abstract

Abstract. Autophagy is a cellular process leading to the degradation of cytoplasmic components such as organelles and intracellular pathogens. It has been shown that HIV-1 relies on several components of the autophagy pathway for its replication, but the virus also blocks late steps of autophagy to prevent its degradation. We generated stable knockdown T cell lines for 12 autophagy factors and analyzed the impact on HIV-1 replication. RNAi-mediated knockdown of 5 autophagy factors resulted in inhibition of HIV-1 replication. Autophagy analysis confirmed a specific defect in the autophagy pathway for 4 of these 5 factors. We also scored the impact on cell viability, but no gross effects were observed. Upon simultaneous knockdown of 2 autophagy factors (Atg16 and Atg5), an additive inhibitory effect was scored on HIV-1 replication. Stable knockdown of several autophagy factors inhibit HIV-1 replication without any apparent cytotoxicity. We therefore propose that targeting of the autophagy pathway can be a novel therapeutic approach against HIV-1

Topics: Antiviral, Autophagy, HIV-1, RNAi
Year: 2012
DOI identifier: 10.1186/1743-422X-9-69
OAI identifier: oai:repub.eur.nl:71795

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