Mechanism and factors that control HIV-1 transcription and latency activation

J Zhejiang Univ Sci B. 2014 May;15(5):455-65. doi: 10.1631/jzus.B1400059.

Abstract

After reverse transcription, the HIV-1 proviral DNA is integrated into the host genome and thus subjected to transcription by the host RNA polymerase II (Pol II). With the identification and characterization of human P-TEFb in the late 1990 s as a specific host cofactor required for HIV-1 transcription, it is now believed that the elongation stage of Pol II transcription plays a particularly important role in regulating HIV-1 gene expression. HIV-1 uses a sophisticated scheme to recruit human P-TEFb and other cofactors to the viral long terminal repeat (LTR) to produce full-length HIV-1 transcripts. In this process, P-TEFb is regulated by the reversible association with various transcription factors/cofactors to form several multi-subunit complexes (e.g., 7SK snRNP, super elongation complexes (SECs), and the Brd4-P-TEFb complex) that collectively constitute a P-TEFb network for controlling cellular and HIV-1 transcription. Recent progresses in HIV-1 transcription were reviewed in the paper, with the emphasis on the mechanism and factors that control HIV-1 transcription and latency activation.

Keywords: HIV-1; P-TEFb; RNA polymerase II; Tat; Transcriptional elongation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Nucleus / physiology
  • Cell Nucleus / virology*
  • DNA, Viral / genetics*
  • Gene Expression Regulation, Viral / genetics*
  • HIV-1 / genetics*
  • Humans
  • Models, Genetic
  • RNA Polymerase II / genetics
  • Transcriptional Activation / genetics*
  • Virus Integration / genetics*
  • Virus Latency / genetics*

Substances

  • DNA, Viral
  • RNA Polymerase II