NDLI: Tat-induced FOXO3a is a key mediator of apoptosis in HIV-1-infected human CD4+ T lymphocytes.

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Tat-induced FOXO3a is a key mediator of apoptosis in HIV-1-infected human CD4+ T lymphocytes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dabrowska, Alicja Kim, Nayoung Aldovini, Anna
Description	Country affiliation: United States Author Affiliation: Dabrowska A ( Department of Medicine, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115, USA.)
Abstract	The high mutation rate of HIV is linked to the generation of viruses expressing proteins with altered function whose impact on disease progression is unknown. We investigated how HIV-1 viruses lacking Env, Vpr, and Nef affect CD4(+) T cell survival. We found that in the absence of these proteins, HIV-1-infected CD4(+) primary T cells progress to the G(0) phase of the cell cycle and to cell death, indicating that viruses expressing inactive forms of these proteins can contribute to the CD4(+) T cell decline as the wild-type virus, suggesting that other HIV proteins are responsible for inducing apoptosis. Apoptosis in these cells is triggered by the alteration of the Egr1-PTEN-Akt (early growth response-1/phosphate and tensin homolog deleted on chromosome 10/Akt) and p53 pathways, which converge on the FOXO3a (Forkhead box transcription factor O class 3a) transcriptional activator. The FOXO3a target genes Fas ligand and TRAIL, involved in the extrinsic apoptotic pathway, and PUMA, Noxa, and Bim, which are part of the intrinsic apoptotic pathway, were also up-regulated, indicating that HIV infection leads to apoptosis by the engagement of multiple apoptotic pathways. RNAi-mediated knockdown of Egr1 and FOXO3a resulted in reduced apoptosis in HIV-infected HeLa and CD4(+) T cells, providing further evidence for their critical role in HIV-induced apoptosis and G(0) arrest. We tested the possibility that Tat is responsible for the T cell apoptosis observed with these mutant viruses. The induction of Egr1 and FOXO3a and its target genes was observed in Jurkat cells transduced by Tat alone. Tat-dependent activation of the Egr1-PTEN-FOXO3a pathway provides a mechanism for HIV-1-associated CD4(+) T cell death.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	12
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-12-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Apoptosis Regulatory Proteins Physiology Apoptosis Immunology Cd4-positive T-lymphocytes Pathology Virology Forkhead Transcription Factors Hiv-1 Tat Gene Products, Human Immunodeficiency Virus Biosynthesis Genetics Metabolism Cell Line Hela Cells Jurkat Cells G0 Phase Env Gene Products, Human Immunodeficiency Virus Deficiency Nef Gene Products, Human Immunodeficiency Virus Vpr Gene Products, Human Immunodeficiency Virus Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Tat-induced FOXO3a is a key mediator of apoptosis in HIV-1-infected human CD4+ T lymphocytes.