NF-kappa B-dependent and -independent pathways of HIV activation in a chronically infected T cell line

Abstract

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