期刊
JOURNAL OF LEUKOCYTE BIOLOGY
卷 83, 期 3, 页码 718-727出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1189/jlb.0607405
关键词
LTR stimulation; viral reservoir; AIDS pathogenesis
HIV-1 two-exon transactivator protein (Tat) is a 101-aa protein. We investigated the possible contribution of the extreme C terminus of HIV-1 Tat to maximize nuclear transcription factor NF-kappa B activation, long terminal repeat (LTR) transactivation, and viral replication in T cells. C-terminal deletion and substitution mutants made with the infectious clone HIV-89.6 were assayed for their ability to transactivate NF-kappa B-secreted alkaline phosphatase and HIV-1 LTR-luciferase reporter constructs for low concentrations of Tat. A mutant infectious clone of HIV-89.6 engineered by introducing a stop codon at aa 72 in the Tat open-reading frame (HIV Delta tatexon2) replicated at a significantly lower rate than the wild-type HIV-89.6 in phytohemagglutinin-A/IL-2-stimulated primary peripheral blood lymphocytes. Altogether, our results suggest a critical role for the glutamic acids at positions 92, 94, and 96 or lysines at positions 88, 89, and 90, present in the second encoding Tat exon in activating NF-kappa B, transactivating the HIV-1 LTR and enhancing HIV-1 replication in T cells.
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