ArticleRedox biology2018
HIV-1 Tat protein induces DNA damage in human peripheral blood B-lymphocytes via mitochondrial ROS production.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 99 citations in OpenAlex.
- Reactive oxygen species (ROS) research in drug discovery and drug delivery: Can the medium Be a Trojan Horse disguised as something benign?Journal of enzyme inhibition and medicinal chemistry · 2026Article
- One Stone Two Birds: Novel Fluorescent Probe Chemistry That Detects Redox Stress in Cell Culture.Analytical chemistry · 2026Article
- HIV and Cancer: Insights into Viral-Mediated Oncogenesis and Immunosuppression.Pathogens (Basel, Switzerland) · 2026Review
- Interaction between HIV-1 Tat and EBV Zta favours immune escape of B cells by downregulating HLA-ABC expression.Cellular and molecular life sciences : CMLS · 2026Article
- Immune Dysregulation in HIV-TB Co-Infection: Role of Cytokines and T Cell Biomarkers-A Narrative Review.Pathogens (Basel, Switzerland) · 2026Review
- HIV reservoirs in lymphomagenesis: hidden driver in the era of viral suppression?Microbiology and molecular biology reviews : MMBR · 2025Review
- Beyond Protection: The Cytotoxic Effect of Anti-Tat Antibodies in People Living with HIV.International journal of molecular sciences · 2025Article
- Detection and Analysis of Reactive Oxygen Species (ROS): Buffer Components Are Not Bystanders.Analytical chemistry · 2025Article
- Oxidative Stress in HIV-Associated Neurodegeneration: Mechanisms of Pathogenesis and Therapeutic Targets.International journal of molecular sciences · 2025Review
- Circulating Biomarker Panorama in HIV-Associated Lymphoma: A Bridge from Early Risk Warning to Prognostic Stratification.Biomolecules · 2025Review
- Article
- Effects of oxidative stress on viral infections: an overview.Npj viruses · 2025Review
- HIV-1 Tat Impairment of Mitochondrial Respiration via Complexes I and II Can Be Ameliorated by Allopregnanolone in Opioid-Exposed or Opioid-Naïve Cells and Mice.Antioxidants (Basel, Switzerland) · 2025Article
- Viruses and the Brain-A Relationship Prone to Trouble.Viruses · 2025Review
- Genotoxic consequences of viral infections.Npj viruses · 2025Review
- Ventricular volume adjustment of brain regions depicts brain changes associated with HIV infection and aging better than intracranial volume adjustment.Frontiers in neurology · 2025Article
- HIV-Tat upregulates the expression of senescence biomarkers in CD4Frontiers in immunology · 2025Article
- IFIT3 activation significantly contributes to HIV-1-associated neurodegenerative disorder-mediated neuroinflammation.Frontiers in immunology · 2025Article
- Mitochondrial DNA damage in HIV infection: a mechanistic driver of immunometabolic dysfunction and chronic inflammation.Frontiers in immunology · 2025Review
- Compensatory reactions of B cells in response to chronic HIV-1 Tat exposure.Journal of cellular physiology · 2025Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human immunodeficiency virus (HIV) infection is associated with B-cell malignancies in patients though HIV-1 is not able to infect B-cells. The rate of B-cell lymphomas in HIV-infected individuals remains high even under the combined antiretroviral therapy (cART) that reconstitutes the immune function. Thus, the contribution of HIV-1 to B-cell oncogenesis remains enigmatic. HIV-1 induces oxidative stress and DNA damage in infected cells via multiple mechanisms, including viral Tat protein. We have detected elevated levels of reactive oxygen species (ROS) and DNA damage in B-cells of HIV-infected individuals. As Tat is present in blood of infected individuals and is able to transduce cells, we hypothesized that it could induce oxidative DNA damage in B-cells promoting genetic instability and malignant transformation. Indeed, incubation of B-cells isolated from healthy donors with purified Tat protein led to oxidative stress, a decrease in the glutathione (GSH) levels, DNA damage and appearance of chromosomal aberrations. The effects of Tat relied on its transcriptional activity and were mediated by NF-κB activation. Tat stimulated oxidative stress in B-cells mostly via mitochondrial ROS production which depended on the reverse electron flow in Complex I of respiratory chain. We propose that Tat-induced oxidative stress, DNA damage and chromosomal aberrations are novel oncogenic factors favoring B-cell lymphomas in HIV-1 infected individuals.
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