ArticleAging cell2015
The HIV proteins Tat and Nef promote human bone marrow mesenchymal stem cell senescence and alter osteoblastic differentiation.
Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 79 citations in OpenAlex.
- In-utero exposure to tenofovir-containing pre-exposure prophylaxis and bone mineral content in HIV-unexposed infants in South Africa.Journal of the International AIDS Society · 2024Trial
- Relationships Between Physical Activity and Bone Density in People Living with HIV: Results from the SATURN-HIV Study.The Journal of the Association of Nurses in AIDS Care : JANACTrial
- Associations Between Immune Senescence and Immune Reconstitution Among People Living With HIV Undergoing Antiretroviral Therapy.Journal of immunology research · 2026Article
- Role of Cytokines in Bone Diseases and Their Therapeutic Application.ImmunoTargets and therapy · 2026Review
- [Mechanism and significance of cell senescence induced by viral infection].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025Review
- Breaking Down Bone Disease in People Living with HIV: Pathophysiology, Diagnosis, and Treatment.Advances in experimental medicine and biology · 2025Review
- Mitochondria: a key regulator of programmed cell death in OP.Frontiers in endocrinology · 2025Review
- HIV-Tat upregulates the expression of senescence biomarkers in CD4Frontiers in immunology · 2025Article
- HIV Modulates Osteoblast Differentiation via Upregulation of RANKL and Vitronectin.Pathogens (Basel, Switzerland) · 2024Article
- Bone Tissue Changes in Individuals Living with HIV/AIDS: The Importance of a Hierarchical Approach in Investigating Bone Fragility.Journal of personalized medicine · 2024Review
- Unilateral avascular necrosis of the right hip in an HIV patient with tearing of the rectus femoris and adductor longus muscles.BMJ case reports · 2024Article
- Bone Disease in HIV: Need for Early Diagnosis and Prevention.Life (Basel, Switzerland) · 2024Review
- Review
- Nucleocapsid Protein (N) ofViruses · 2023Article
- Involvement of lncRNA TUG1 in HIV-1 Tat-Induced Astrocyte Senescence.International journal of molecular sciences · 2023Article
- Consequences of HIV infection in the bone marrow niche.Frontiers in immunology · 2023Review
- Massively HIV-1-infected macrophages exhibit a severely hampered ability to differentiate into osteoclasts.Frontiers in immunology · 2023Article
- Senotherapeutics: An emerging approach to the treatment of viral infectious diseases in the elderly.Frontiers in cellular and infection microbiology · 2023Review
- Bone Quality in Relation to HIV and Antiretroviral Drugs.Current HIV/AIDS reports · 2022Review
- Parvovirus B19 induces cellular senescence in human dermal fibroblasts: putative role in systemic sclerosis-associated fibrosis.Rheumatology (Oxford, England) · 2022Article
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To maintain bone mass turnover and bone mineral density (BMD), bone marrow (BM) mesenchymal stem cells (MSCs) are constantly recruited and subsequently differentiated into osteoblasts. HIV-infected patients present lower BMD than non-HIV infected individuals and a higher prevalence of osteopenia/osteoporosis. In antiretroviral treatment (ART)-naive patients, encoded HIV proteins represent pathogenic candidates. They are released by infected cells within BM and can impact on neighbouring cells. In this study, we tested whether HIV proteins Tat and/or Nef could induce senescence of human BM-MSCs and reduce their capacity to differentiate into osteoblasts. When compared to nontreated cells, MSCs chronically treated with Tat and/or Nef up to 30 days reduced their proliferative activity and underwent early senescence, associated with increased oxidative stress and mitochondrial dysfunction. The antioxidant molecule N-acetyl- cysteine had no or minimal effects on Tat- or Nef-induced senescence. Tat but not Nef induced an early increase in NF-κB activity and cytokine/chemokine secretion. Tat-induced effects were prevented by the NF-κB inhibitor parthenolide, indicating that Tat triggered senescence via NF-κB activation leading to oxidative stress. Otherwise, Nef- but not Tat-treated cells displayed early inhibition of autophagy. Rapamycin, an autophagy inducer, reversed Nef-induced senescence and oxidative stress. Moreover, Tat+Nef had cumulative effects. Finally, Tat and/or Nef decreased the MSC potential of osteoblastic differentiation. In conclusion, our in vitro data show that Tat and Nef could reduce the number of available precursors by inducing MSC senescence, through either enhanced inflammation or reduced autophagy. These results offer new insights into the pathophysiological mechanisms of decreased BMD in HIV-infected patients.
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