Specific sequence configurations of HIV-1 LTR G/C box array result in altered recruitment of Sp isoforms and correlate with disease progression

J Neuroimmunol. 2004 Dec;157(1-2):39-47. doi: 10.1016/j.jneuroim.2004.08.021.

Abstract

Basal and activated human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) activity, and in return, viral replication is partly dependent on interactions of the G/C box array with the Sp family of transcription factors. Analysis of LTR Sp binding site sequence variants revealed a C-to-T change at position 5 within Sp site III that increased in frequency and a 5T mutation within Sp site II, which decreased in frequency during the course of HIV disease. These results suggest LTR Sp binding site sequence variants may prove useful as viral molecular markers indicative of progressive HIV-1-induced disease.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Base Sequence / physiology
  • Binding Sites / drug effects
  • Binding Sites / physiology
  • Cell Line
  • Chi-Square Distribution
  • Consensus Sequence / genetics
  • Disease Progression
  • Electrophoretic Mobility Shift Assay / methods
  • HIV Infections / pathology*
  • HIV Long Terminal Repeat / genetics*
  • Humans
  • Mutation / genetics
  • NF-kappa B / physiology
  • Oligonucleotides / pharmacology
  • Promoter Regions, Genetic / genetics*
  • Protein Binding / drug effects
  • Protein Binding / genetics
  • Sp1 Transcription Factor / genetics*
  • Virus Replication / physiology*

Substances

  • NF-kappa B
  • Oligonucleotides
  • Sp1 Transcription Factor