Intracellular high mobility group B1 protein (HMGB1) represses HIV-1 LTR-directed transcription in a promoter- and cell-specific manner

Mojgan H. Naghavi*, Piotr Nowak, Jan Andersson, Anders Sönnerborg, Huan Yang, Kevin J. Tracey, Anders Vahlne

*Corresponding author for this work

Research output: Contribution to journalArticle

34 Scopus citations

Abstract

We investigated whether the high mobility group B 1 (HMGB1), an abundant nuclear protein in all mammalian cells, affects HIV-1 transcription. Intracellular expression of human HMGB1 repressed HIV-1 gene expression in epithelial cells. This inhibitory effect of HMGB1 was caused by repression of long terminal repeat (LTR)-mediated transcription. Other viral promoters/enhancers, including simian virus 40 or cytomegalovirus, were not inhibited by HMGB1. In addition, HMGB1 inhibition of HIV-1 subtype C expression was dependent on the number of NFκB sites in the LTR region. The inhibitory effect of HMGB1 on viral gene expression observed in HeLa cells was confirmed by an upregulation of viral replication in the presence of antisense HMGB1 in monocytic cells. In contrast to what was found in HeLa cells and monocytic cells, endogenous HMGB1 expression did not affect HIV-1 replication in unstimulated Jurkat cells. Thus, intracellular HMGB1 affects HIV-1 LTR-directed transcription in a promoter- and cell-specific manner.

Original languageEnglish (US)
Pages (from-to)179-189
Number of pages11
JournalVirology
Volume314
Issue number1
DOIs
StatePublished - Sep 15 2003

Keywords

  • HIV-1 subtypes
  • HMGB1
  • LTR
  • Rel proteins
  • Transcription

ASJC Scopus subject areas

  • Virology

Fingerprint Dive into the research topics of 'Intracellular high mobility group B1 protein (HMGB1) represses HIV-1 LTR-directed transcription in a promoter- and cell-specific manner'. Together they form a unique fingerprint.

  • Cite this