TFII-I Regulates Induction of Chromosomally Integrated Human Immunodeficiency Virus Type 1 Long Terminal Repeat in Cooperation with USF

Abstract

Human immunodeficiency virus type 1 (HIV-1) replication is coupled to T-cell activation through its dependence on host cell transcription factors. Despite the enormous sequence variability of these factors, several cis elements for host factors are highly conserved within the 5 long terminal repeats (LTRs) of viruses from AIDS patients; among these is the RBEIII upstream element for the Ras response element binding factor 2 (RBF-2). Here we show that RBF-2 is comprised of a USF1/USF2 heterodimer and TFII-I, which bind cooperatively to RBEIII. Recombinant USF1/USF2 binds to the RBEIII core sequence 160-fold less efficiently than it binds to an E box element, but the interaction with RBEIII is stimulated by TFII-I. Chromosomally

Duplicated Sequence Motif in the Long Terminal Repeat of Maedi-Visna Virus Extends Cell Tropism and Is Associated with Neurovirulence

“…Our finding that both the CAAAT sequence and the AML site, when present in one copy, contribute to the transcription efficiency in SCP cells further supports the notion that transcription is synergistically controlled by a repertoire of transcription factors and that the repeated sequence creates a redundancy of transcription factor binding sites (25). The loss of virus replication that we detected in this study may be controlled at the level of chromatin that cannot be detected by transient transfection (12,33). Chromatin remodeling has been shown to modulate gene expression, and in fact, there is increasing evidence that the lentiviruses are regulated at the level of chromosomally integrated virus (9,12,26,27,53).…”

“…The loss of virus replication that we detected in this study may be controlled at the level of chromatin that cannot be detected by transient transfection (12,33). Chromatin remodeling has been shown to modulate gene expression, and in fact, there is increasing evidence that the lentiviruses are regulated at the level of chromosomally integrated virus (9,12,26,27,53).…”

TRIM22 Inhibits HIV-1 Transcription Independently of Its E3 Ubiquitin Ligase Activity, Tat, and NF-κB-Responsive Long Terminal Repeat Elements

“…In contrast to Tat and the NF-B-dependent pathways, PϩI-induced signaling was found to be sensitive to the inhibitory effects of TRIM22. In this regard, PϩI can trigger signal pathways leading to activation of a broad array of transcription factors, including AP-1 and NFAT (13), that, together with constitutively expressed Sp1, play a crucial role in the early triggering of HIV-1 transcription (36,58,67,78,80). Interestingly, PϩI-mediated activation of the viral LTR has been reported to strongly depend on an intact RBEIII region at position Ϫ120 of the viral promoter, harboring the binding site for RBF-2 (USF1/2-TFII-I) (41).…”

Identification of Cellular Proteins Required for Replication of Human Immunodeficiency Virus Type 1

“…35,36 Although several TFIIs have been shown to stimulate HIV-1 transcription including TFIID, TFIIF, TFIIH, and TFII-I, [37][38][39][40] the importance of TFIIE has not been demonstrated. We found that both the a and b subunits of TFIIE (GTF2E1 and GTF2E2, respectively) support replication with R5-, R5X4-, and X4-tropic strains in TZM-bl cells (Figs.…”