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

Michael R. Nonnemacher, Bryan P. Irish, Yujie Liu, David Mauger, Brian Wigdahl

Research output: Contribution to journalArticle

18 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)39-47
Number of pages9
JournalJournal of Neuroimmunology
Volume157
Issue number1-2 SPEC. ISS.
DOIs
StatePublished - Dec 1 2004

Fingerprint

HIV Long Terminal Repeat
Terminal Repeat Sequences
Disease Progression
HIV-1
Sp Transcription Factors
Protein Isoforms
Binding Sites
Biomarkers
HIV
Mutation

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

Cite this

Nonnemacher, Michael R. ; Irish, Bryan P. ; Liu, Yujie ; Mauger, David ; Wigdahl, Brian. / Specific sequence configurations of HIV-1 LTR G/C box array result in altered recruitment of Sp isoforms and correlate with disease progression. In: Journal of Neuroimmunology. 2004 ; Vol. 157, No. 1-2 SPEC. ISS. pp. 39-47.
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Specific sequence configurations of HIV-1 LTR G/C box array result in altered recruitment of Sp isoforms and correlate with disease progression. / Nonnemacher, Michael R.; Irish, Bryan P.; Liu, Yujie; Mauger, David; Wigdahl, Brian.

In: Journal of Neuroimmunology, Vol. 157, No. 1-2 SPEC. ISS., 01.12.2004, p. 39-47.

Research output: Contribution to journalArticle

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AU - Wigdahl, Brian

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