title: Oxaliplatin antagonizes HIV-1 latency by activating NF-κB without causing global T cell activation.
abstract: Reactivation of latent HIV-1 is a promising strategy for the clearance of the viral reservoirs. Because of the limitations of current agents, identification of new latency activators is urgently required. Using an established model of HIV-1 latency, we examined the effect of Oxaliplatin on latent HIV-1 reactivation. We showed that Oxaliplatin, alone or in combination with valproic acid (VPA), was able to reactivate HIV-1 without inducing global T cell activation. We also provided evidence that Oxaliplatin reactivated HIV-1 expression by inducing nuclear factor kappa B (NF-κB) nuclear translocation. Our results indicated that Oxaliplatin could be a potential drug candidate for anti-latency therapies.
authors.affiliation: State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, China.
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Zhu
authors.affiliation: State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, China.
authors.forename: Sijie
authors.initials: S
authors.lastname: Liu
authors.affiliation: State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, China.
authors.forename: Pengfei
authors.initials: P
authors.lastname: Wang
authors.affiliation: State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, China.
authors.forename: Xiying
authors.initials: X
authors.lastname: Qu
authors.affiliation: State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, China.
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Wang
authors.affiliation: State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, China.
authors.forename: Hanxian
authors.initials: H
authors.lastname: Zeng
authors.affiliation: Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard University, Cambridge, MA 02139, USA.
authors.forename: Huabiao
authors.initials: H
authors.lastname: Chen
authors.affiliation: State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, China. Electronic address: hzzhu@fudan.edu.cn.
authors.forename: Huanzhang
authors.initials: H
authors.lastname: Zhu
mesh_terms: D002478:Cells, Cultured; D015497:HIV-1 / Q000187:drug effects / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation / Q000187:drug effects / Q000276:immunology*; D016328:NF-kappa B / Q000276:immunology*; D009944:Organoplatinum Compounds / Q000494:pharmacology*; D000077150:Oxaliplatin; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology* / Q000821:virology*; D014775:Virus Activation / Q000187:drug effects / Q000276:immunology*; D017735:Virus Latency / Q000187:drug effects / Q000276:immunology*
chemical_list: D016328:NF-kappa B; D009944:Organoplatinum Compounds; D000077150:Oxaliplatin
keywords: HIV-1 latency; NF-κB transcription factor; Oxaliplatin; Synergistic reactivation