TY - JOUR
AU - Peterlin, M B
AB -  The human immunodeficiency virus (HIV) is a highly pathogenic lentivirus that causes acquired immune deficiency syndrome (AIDS) ( 1-3). Since the first sequence analyses of HIV-l were reported in 1985 (4--6), a wealth of 717 0066-4154/94/0701-0717$05.00 JONES & PETERLIN information has accrued on the steps that regulate viral gene expression in infected cells. HIV-l infection is characterized by a lengthy period of proviral latency during which few viral transcripts or regulatory proteins are produced. Much of this regulation is transcriptional, exerted through the viral promoter located in the leftward long terminal repeat (LTR). Most notably, RNA polymerase II (RNA pol II) transcription complexes that are initiated from the viral promoter early in infection terminate RNA synthesis prematurely through a process of attenuation or abortive elongation. HIV-l encodes six regulatory proteins that control different aspects of the viral life cycle, from virus entry and reverse transcription to transcription of the integrated provirus and nuclear transport of unspliced viral RNAs. One of the earliest regulatory proteins, Tat (7-9), is an essential nuclear protein that is targeted to the viral promoter through a nascent RNA signal to activate transcription. Tat strongly increases t�e efficiency or processivity of elongation by RNA polymerase 
TI - Control of RNA Initiation and Elongation at the HIV-1 Promoter
JF - Annual Review of Biochemistry
DO - 10.1146/annurev.bi.63.070194.003441
DA - 1994-07-01
UR - https://www.deepdyve.com/lp/annual-reviews/control-of-rna-initiation-and-elongation-at-the-hiv-1-promoter-DjWSo0j3lP
SP - 717
EP - 743
VL - 63
IS - 1
DP - DeepDyve
ER -