A novel Ets-related transcription factor, Elf-1, binds to human immunodeficiency virus type 2 regulatory elements that are required for inducible trans activation in T cells

Jeffrey M. Leiden, Chung Yih Wang, Bronislawa Petryniak, David M. Markovitz, Gary J. Nabel, Craig B. Thompson

Research output: Contribution to journalArticlepeer-review

87 Scopus citations

Abstract

Human immunodeficiency virus type 1 (HIV-1) and HIV-2 are structurally related retroviruses which both cause AIDS in humans. Although both viruses establish latency in quiescent human-peripheral-blood T cells, the asymptomatic phase of HIV-2 infection may be more prolonged than that of HIV-1. The latent phases of both HIV-1 and HIV-2 infection have been shown to be disrupted by T-cell activation, a process that requires host cell transcription factors. In the case of HIV-1, the transcription factor NF-κB is sufficient for inducible transcriptional activation. In contrast, factors in addition to NF-κB are required to activate HIV-2 transcription in infected T cells. In this report, we demonstrate that a novel Ets-related transcription factor, Elf-1, binds specifically to two purine-rich motifs in the HIV-2 enhancer. Mutagenesis experiments demonstrated that these Elf-1 binding sites are required for induction of HIV-2 transcription following T-cell-receptor-mediated T-cell activation. Moreover, Elf-1 is the only factor present in activated T-cell nuclear extracts that binds to these sites in electrophoretic mobility shift assays. Thus, Elf-1 is a novel transcription factor that appears to be required for the T-cell-receptor-mediated trans activation of HIV-2 gene expression. These results may explain differences in the clinical spectra of diseases caused by HIV-1 and HIV-2 and may also have implicatioas for the design of therapeutic approaches to HIV-2 infection.

Original languageEnglish (US)
Pages (from-to)5890-5897
Number of pages8
JournalJournal of Virology
Volume66
Issue number10
StatePublished - Oct 1992
Externally publishedYes

ASJC Scopus subject areas

  • Immunology

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