Document Type
Article
Publication Date
3-8-2021
Abstract
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-κB, 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-κB enhances HIV transcription while NFAT inhibits it by competing with NF-κB 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-κB to regulate HIV transcriptional elongation following TCR activation.
Recommended Citation
Hokello, Joseph; Sharma, Adhikarimayum Lakhikumar; and Tyagi, Mudit, "AP-1 and NF-κB synergize to transcriptionally activate latent HIV upon T-cell receptor activation." (2021). Center for Translational Medicine Faculty Papers. Paper 91.
https://jdc.jefferson.edu/transmedfp/91
PubMed ID
33421101
Language
English
Comments
This is the peer reviewed version of the following article:
Hokello, J., Lakhikumar Sharma, A. and Tyagi, M. (2021), AP-1 and NF-κB synergize to transcriptionally activate latent HIV upon T-cell receptor activation. FEBS Lett, 595: 577-594.
It has been published in final form at https://doi.org/10.1002/1873-3468.14033. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.