NF-κ B-Dependent and -Independent Pathways of HIV Activation in a Chronically Infected T Cell Line

Beth Ann Antoni, Arnold Rabson, Audrey Kinter, Marlon Bodkin, Guido Poli

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

JΔK cells were isolated as a chronically infected survivor cell line, following infection of Jurkat CD4+ T cells with dI-NF, a mutated strain of human immunodeficiency virus type 1 (HIV-1) containing a deletion of the long terminal repeat (LTR) NF-κB sites. JΔK cells exhibited very low levels of constitutive HIV production. HIV-1 expression was activated from JΔK cells by treatment with phorbol myristate acetate (PMA), sodium butyrate (NAB), or hexamethylene bisacetamide (HMBA), but not tumor necrosis factor α (TNF-α), confirming the role of NF-κB in mediating TNF-α induction of HIV transcription. The strong induction of HIV expression by NaB or HMBA in JΔK cells clearly demonstrates the existence of NF-κB-independent mechanisms of HIV activation in chronically infected cells. JΔK cells may provide a useful model for characterizing NF-κB-independent transcriptional activation of the HIV LTR.

Original languageEnglish (US)
Article number71390
Pages (from-to)684-694
Number of pages11
JournalVirology
Volume202
Issue number2
DOIs
StatePublished - Aug 1 1994

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hexamethylene bisacetamide
HIV
T-Lymphocytes
Cell Line
HIV-1
Tumor Necrosis Factor-alpha
HIV Long Terminal Repeat
Butyric Acid
Terminal Repeat Sequences
Tetradecanoylphorbol Acetate
Transcriptional Activation
Infection

All Science Journal Classification (ASJC) codes

  • Virology

Cite this

Antoni, Beth Ann ; Rabson, Arnold ; Kinter, Audrey ; Bodkin, Marlon ; Poli, Guido. / NF-κ B-Dependent and -Independent Pathways of HIV Activation in a Chronically Infected T Cell Line. In: Virology. 1994 ; Vol. 202, No. 2. pp. 684-694.
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NF-κ B-Dependent and -Independent Pathways of HIV Activation in a Chronically Infected T Cell Line. / Antoni, Beth Ann; Rabson, Arnold; Kinter, Audrey; Bodkin, Marlon; Poli, Guido.

In: Virology, Vol. 202, No. 2, 71390, 01.08.1994, p. 684-694.

Research output: Contribution to journalArticle

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