Host control of HIV-1 parasitism in T cells by the nuclear factor of activated T cells.

Important note: Information in this article was accurate in 1999. The state of the art may have changed since the publication date.

Host control of HIV-1 parasitism in T cells by the nuclear factor of activated T cells.

Unique Identifier : AIDSLINE MED/99059495
Kinoshita S; Chen BK; Kaneshima H; Nolan GP; Department of Molecular Pharmacology, Stanford University School; of Medicine, California 94305, USA.

Abstract: Post HIV-1 entry, productive HIV-1 infection of primary T cells requires overcoming several cellular blocks to provirus establishment and replication. Activation of unknown host intracellular events overcomes such inhibitory steps and is concomitant with HIV-1 replication. We show that the transcription factor NFATc was sufficient as a cellular factor to induce a highly permissive state for HIV-1 replication in primary CD4+ T cells. NFATc overcame a blockade at reverse transcription and permitted active HIV-1 replication. Pharmacologic blockade of endogenous NFAT activity by FK506 or CsA inhibited synthesis of reverse transcription and also potently blocked HIV-1 replication. T cells therefore can become competent for HIV-1 replication by control of regulated host factors such as the NFATc transcription factor. The host mechanisms regulated by such permissivity factors are potential targets for anti-HIV-1 therapy.

Keywords: JOURNAL ARTICLE Cell Division Cells, Cultured Cyclosporine/PHARMACOLOGY CD4-Positive T-Lymphocytes/IMMUNOLOGY/VIROLOGY DNA-Binding Proteins/*PHYSIOLOGY Human HIV Infections/*IMMUNOLOGY HIV-1/PHYSIOLOGY/*PATHOGENICITY
990330
A9931088

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