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-I) containing a deletion of the long terminal repeat (LTR) NF-KB 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-KB 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-kB-independent mechanisms of HIV activation in chronically infected cells. J Delta K cells may provide a useful model for characterizing NF-kB-independent transcriptional activation of the HIV LTR. (C) 1994 Academic Press, Inc.

NF-KAPPA-B-DEPENDENT AND NF-KAPPA-B-INDEPENDENT PATHWAYS OF HIV ACTIVATION IN A CHRONICALLY INFECTED T-CELL LINE

POLI , GUIDO
1994

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-I) containing a deletion of the long terminal repeat (LTR) NF-KB 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-KB 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-kB-independent mechanisms of HIV activation in chronically infected cells. J Delta K cells may provide a useful model for characterizing NF-kB-independent transcriptional activation of the HIV LTR. (C) 1994 Academic Press, Inc.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11768/7753
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