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- W98617097 abstract "HIV-1 replication in primary human CD4+T cells requires cellular activation and host cholesterol for productive infection. Interestingly, both T cell activation and HIV-1 infection independently induce SREBP-2-dependent transcription. Oxysterols that suppress host cell cholesterol-dependent transcription by inhibiting SREBP-2 processing also inhibit HIV-1 replication in vitro. Using bioinformatic and molecular approaches, we have identified TFII-I, a transcription factor critical for T cell receptor-mediated HIV-1 LTR transcription, as a novel SREBP-2 target gene in CD4+T cells. Levels of TFII-I in CD4+T cells increased after HIV-1 infection and correlated with the level of T cell activation. Reduction of endogenous SREBP-2 activity by 25-hydroxycholesterol treatment or siRNA-mediated silencing inhibited induction of TFII-I in both activated and HIV-1 infected primary CD4+T cells. Correspondingly, depletion of SREBP-2 reduced HIV-1 replication in CD4+T cells by more than 75%. Consistent with a role in HIV-1 LTR transcription, siRNA-mediated knockdown of either SREBP-2 or TFII-I reduced intracellular viral antigen levels in HIV-1-infected CD4+T cells. Collectively, these results demonstrate that control of TFII-I expression via SREBP-2 is essential for HIV-1 replication. Inhibition of this pathway may provide a new therapeutic strategy for AIDS. Supported by NIH (R01 HD040772)" @default.
- W98617097 created "2016-06-24" @default.
- W98617097 creator A5031009872 @default.
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- W98617097 date "2009-04-01" @default.
- W98617097 modified "2023-09-26" @default.
- W98617097 title "Sterol regulatory element‐binding protein 2 (SREBP‐2) couples cholesterol homeostasis and T cell activation to HIV‐1 transcription" @default.
- W98617097 doi "https://doi.org/10.1096/fasebj.23.1_supplement.537.2" @default.
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