ArticleRetrovirology2015
Intracellular expression of Tat alters mitochondrial functions in T cells: a potential mechanism to understand mitochondrial damage during HIV-1 replication.
Article in Retrovirology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 38 citations in OpenAlex.
- HIV-1 Tat and gp120 as key drivers of neurodegeneration in the central nervous system.Frontiers in microbiology · 2026Review
- IL-18 and MIG increase one year after transition to dolutegravir-based dual therapy despite sustained viral suppression.Frontiers in immunology · 2026Article
- HIV-1 viral protein effect on cerebral microvasculature: An in vitro blood-brain barrier model.Physiological reports · 2025Article
- Mitochondrial DNA damage in HIV infection: a mechanistic driver of immunometabolic dysfunction and chronic inflammation.Frontiers in immunology · 2025Review
- Intracellular HIV-1 Tat regulator induces epigenetic changes in the DNA methylation landscape.Frontiers in immunology · 2025Article
- HIV-Tat upregulates the expression of senescence biomarkers in CD4Frontiers in immunology · 2025Article
- Longitudinal changes in mitochondrial-associated measures and insulin resistance in youth with perinatally-acquired HIV in the U.S.Mitochondrion · 2024Article
- Analysis of Sigma-1 Receptor Antagonist BD1047 Effect on Upregulating Proteins in HIV-1-Infected Macrophages Exposed to Cocaine Using Quantitative Proteomics.Biomedicines · 2024Article
- Metabolic, Mitochondrial, and Inflammatory Effects of Efavirenz, Emtricitabine, and Tenofovir Disoproxil Fumarate in Asymptomatic Antiretroviral-Naïve People with HIV.International journal of molecular sciences · 2024Article
- Role of HIV-1 Tat Protein Interactions with Host Receptors in HIV Infection and Pathogenesis.International journal of molecular sciences · 2024Review
- The role of autophagy in the progression of HIV infected cardiomyopathy.Frontiers in cell and developmental biology · 2024Review
- Providing a Helping Hand: Metabolic Regulation of T Follicular Helper Cells and Their Association With Disease.Frontiers in immunology · 2022Review
- HIV-1 Tat and cocaine impact mitochondrial epigenetics: effects on DNA methylation.Epigenetics · 2021Article
- Observational
- HIV and the tuberculosis "set point": how HIV impairs alveolar macrophage responses to tuberculosis and sets the stage for progressive disease.Retrovirology · 2020Review
- Mitochondrial Dysfunction and Insulin Resistance in Pubertal Youth Living with Perinatally Acquired HIV.AIDS research and human retroviruses · 2020Article
- HIV-1 and HIV-1-Tat Induce Mitochondrial DNA Damage in Human Neurons.Journal of HIV and AIDS · 2020Article
- Cellular stress responses and dysfunctional Mitochondrial-cellular senescence, and therapeutics in chronic respiratory diseases.Redox biology · 2020Review
- HIV-1 Tat Length: Comparative and Functional Considerations.Frontiers in microbiology · 2020Article
- Subcutaneous Adipocyte Adenosine Triphosphate Levels in HIV Infected Patients.AIDS research and human retroviruses · 2020Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHIV-1 replication results in mitochondrial damage that is enhanced during antiretroviral therapy (ART). The onset of HIV-1 replication is regulated by viral protein Tat, a 101-residue protein codified by two exons that elongates viral transcripts. Although the first exon of Tat (aa 1-72) forms itself an active protein, the presence of the second exon (aa 73-101) results in a more competent transcriptional protein with additional functions.
resultsMitochondrial overall functions were analyzed in Jurkat cells stably expressing full-length Tat (Tat101) or one-exon Tat (Tat72). Representative results were confirmed in PBLs transiently expressing Tat101 and in HIV-infected Jurkat cells. The intracellular expression of Tat101 induced the deregulation of metabolism and cytoskeletal proteins which remodeled the function and distribution of mitochondria. Tat101 reduced the transcription of the mtDNA, resulting in low ATP production. The total amount of mitochondria increased likely to counteract their functional impairment. These effects were enhanced when Tat second exon was expressed.
conclusionsIntracellular Tat altered mtDNA transcription, mitochondrial content and distribution in CD4+ T cells. The importance of Tat second exon in non-transcriptional functions was confirmed. Tat101 may be responsible for mitochondrial dysfunctions found in HIV-1 infected patients.
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