ArticleJournal of virology2005
Distinct mechanisms of CD4+ and CD8+ T-cell activation and bystander apoptosis induced by human immunodeficiency virus type 1 virions.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- Patterns of inflammation and immune activation by coreceptor use in people living with HIV-1.Frontiers in immunology · 2025Article
- Transcriptome-based analysis of human peripheral blood reveals regulators of immune response in different viral infections.Frontiers in immunology · 2023Article
- Host Molecule Incorporation into HIV Virions, Potential Influences in HIV Pathogenesis.Viruses · 2022Review
- The role of CD38 in HIV infection.AIDS research and therapy · 2021Review
- A computational analysis of transcriptional profiles from CD8(+) T lymphocytes reveals potential mechanisms of HIV/AIDS control and progression.Computational and structural biotechnology journal · 2021Article
- Review
- Immune Activation Influences SAMHD1 Expression and Vpx-mediated SAMHD1 Degradation during Chronic HIV-1 Infection.Scientific reports · 2016Article
- Casp8p41: The Protean Mediator of Death in CD4 T-cells that Replicate HIV.Journal of cell death · 2016Review
- Cell-to-Cell Transmission of HIV-1 Is Required to Trigger Pyroptotic Death of Lymphoid-Tissue-Derived CD4 T Cells.Cell reports · 2015Article
- T-cell activation, both pre- and post-HAART levels, correlates with carotid artery stiffness over 6.5 years among HIV-infected women in the WIHS.Journal of acquired immune deficiency syndromes (1999) · 2014Article
- Deep sequencing of HIV-infected cells: insights into nascent transcription and host-directed therapy.Journal of virology · 2014Article
- A quantitative comparison of anti-HIV gene therapy delivered to hematopoietic stem cells versus CD4+ T cells.PLoS computational biology · 2014Article
- Enhanced innate antiviral gene expression, IFN-α, and cytolytic responses are predictive of mucosal immune recovery during simian immunodeficiency virus infection.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- The majority of CD4+ T-cell depletion during acute simian-human immunodeficiency virus SHIV89.6P infection occurs in uninfected cells.Journal of virology · 2014Article
- Circulating Type-1 Anti-Tumor CD4(+) T Cells are Preferentially Pro-Apoptotic in Cancer Patients.Frontiers in oncology · 2014Article
- Dimorphic HLA-B signal peptides differentially influence HLA-E- and natural killer cell-mediated cytolysis of HIV-1-infected target cells.Clinical and experimental immunology · 2013Article
- Association of HIV clinical disease progression with profiles of early immune activation: results from a cluster analysis approach.AIDS (London, England) · 2013Article
- T-Cell Signaling in HIV-1 Infection.The open virology journal · 2013Article
- Role of apoptosis in disease.Aging · 2012Review
- Pathogen-specific T cell depletion and reactivation of opportunistic pathogens in HIV infection.Trends in immunology · 2012Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Apoptosis of uninfected bystander T cells contributes to T-cell depletion during human immunodeficiency virus type 1 (HIV-1) infection. HIV-1 envelope/receptor interactions and immune activation have been implicated as contributors to bystander apoptosis. To better understand the relationship between T-cell activation and bystander apoptosis during HIV-1 pathogenesis, we investigated the effects of the highly cytopathic CXCR4-tropic HIV-1 variant ELI6 on primary CD4(+) and CD8(+) T cells. Infection of primary T-cell cultures with ELI6 induced CD4(+) T-cell depletion by direct cell lysis and bystander apoptosis. Exposure of primary CD4(+) and CD8(+) T cells to nonreplicating ELI6 virions induced bystander apoptosis through a Fas-independent mechanism. Bystander apoptosis of CD4(+) T cells required direct contact with virions and Env/CXCR4 binding. In contrast, the apoptosis of CD8(+) T cells was triggered by a soluble factor(s) secreted by CD4(+) T cells. HIV-1 virions activated CD4(+) and CD8(+) T cells to express CD25 and HLA-DR and preferentially induced apoptosis in CD25(+)HLA-DR(+) T cells in a CXCR4-dependent manner. Maximal levels of binding, activation, and apoptosis were induced by virions that incorporated MHC class II and B7-2 into the viral membrane. These results suggest that nonreplicating HIV-1 virions contribute to chronic immune activation and T-cell depletion during HIV-1 pathogenesis by activating CD4(+) and CD8(+) T cells, which then proceed to die via apoptosis. This mechanism may represent a viral immune evasion strategy to increase viral replication by activating target cells while killing immune effector cells that are not productively infected.
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