Journal
FEBS LETTERS
Volume 595, Issue 5, Pages 577-594Publisher
WILEY
DOI: 10.1002/1873-3468.14033
Keywords
HIV Latency; HIV transcriptional elongation; TCR activation
Funding
- National Institute on Drug Abuse (NIDA), NIH [1R01DA041746-01]
- Fogarty International Center (FIC) at the National Institutes of Health (NIH) through the Fogarty- AIDS International Training and Research Program (AITRP) [NIH 5D43 TW00011]
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This study reveals the roles of NF-kappa B, NFAT, and AP-1 transcription factors in the reactivation of latent HIV, and the competitive and synergistic relationships between them in regulating HIV transcription.
Latent HIV-1 proviruses are capable of reactivating productive lytic infection, but the precise molecular mechanisms underlying emergence from latency are poorly understood. In this study, we determined the contribution of the transcription factors NF-kappa B, NFAT, and AP-1 in the reactivation of latent HIV following T-cell receptor (TCR) activation using Jurkat T-cell clones harboring single latent HIV proviruses. Our findings demonstrate that during reactivation from latency, NF-kappa B enhances HIV transcription while NFAT inhibits it by competing with NF-kappa B for overlapping binding sites on the HIV long terminal repeat (LTR). We have also demonstrated for the first time the molecular contribution of AP-1 in the reactivation of HIV from latency, whereby AP-1 synergizes with NF-kappa B to regulate HIV transcriptional elongation following TCR activation.
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