ArticleJournal of virology2020
HIV-1 Tat Interacts with a Kaposi's Sarcoma-Associated Herpesvirus Reactivation-Upregulated Antiangiogenic Long Noncoding RNA, LINC00313, and Antagonizes Its Function.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Oral manifestations in HIV-positive individuals under highly active antiretroviral therapy: a systematic review and meta-analysis of prevalence data.BMC oral health · 2026Pooled it
- 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
- Molecular Investigation of Product Nkabinde in HIV Therapy: A Network Pharmacology and Molecular Docking Approach.International journal of molecular sciences · 2026Article
- Risks of replication-competent retro/lentivirus from associated vector systems: Is it time for a roadmap toward reduced testing?Molecular therapy. Methods & clinical development · 2025Review
- Similar Viral and Immune Characteristics of Kaposi Sarcoma in ART-treated People Living With HIV and Older Patients With Classic Kaposi Sarcoma.Open forum infectious diseases · 2024Article
- Review
- Long noncoding RNA study: Genome-wide approaches.Genes & diseases · 2023Review
- LINC00313 promotes the proliferation and inhibits the apoptosis of chondrocytes via regulating miR-525-5p/GDF5 axis.Journal of orthopaedic surgery and research · 2023Article
- The Persistence of HIV Diversity, Transcription, and Nef Protein in Kaposi's Sarcoma Tumors during Antiretroviral Therapy.Viruses · 2022Article
- Long noncoding RNAs (lncRNAs) in HIV-mediated carcinogenesis: Role in cell homeostasis, cell survival processes and drug resistance.Non-coding RNA research · 2022Review
- Epigenetic Changes and Functions in Pneumoconiosis.Oxidative medicine and cellular longevity · 2022Review
- SARS-CoV-2, Cardiovascular Diseases, and Noncoding RNAs: A Connected Triad.International journal of molecular sciences · 2021Review
- New insights into pathogenesis point to HIV-1 Tat as a key vaccine target.Archives of virology · 2021Review
- Long non-coding RNAs and circular RNAs in tumor angiogenesis: From mechanisms to clinical significance.Molecular therapy oncolytics · 2021Review
- HIV-1 Transactivator of Transcription (Tat) Co-operates With AP-1 Factors to EnhanceFrontiers in cell and developmental biology · 2021Article
- Long Non-coding RNAs in Gammaherpesvirus Infections: Their Roles in Tumorigenic Mechanisms.Frontiers in microbiology · 2020Review
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi's sarcoma (KS), an AIDS-defining cancer with abnormal angiogenesis. The high incidence of KS in human immunodeficiency virus (HIV)-infected AIDS patients has been ascribed to an interaction between HIV type 1 (HIV-1) and KSHV, focusing on secretory proteins. The HIV-1 secreted protein HIV Tat has been found to synergize with KSHV lytic proteins to induce angiogenesis. However, the impact and underlying mechanisms of HIV Tat in KSHV-infected endothelial cells undergoing viral lytic reactivation remain unclear. Here, we identified LINC00313 as a novel KSHV reactivation-activated long noncoding RNA (lncRNA) that interacts with HIV Tat. We found that LINC00313 overexpression inhibits cell migration, invasion, and tube formation, and this suppressive effect was relieved by HIV Tat. In addition, LINC00313 bound to polycomb repressive complex 2 (PRC2) complex components, and this interaction was disrupted by HIV Tat, suggesting that LINC00313 may mediate transcription repression through recruitment of PRC2 and that HIV Tat alleviates repression through disruption of this association. This notion was further supported by bioinformatics analysis of transcriptome profiles in LINC00313 overexpression combined with HIV Tat treatment. Ingenuity Pathway Analysis (IPA) showed that LINC00313 overexpression negatively regulates cell movement and migration pathways, and enrichment of these pathways was absent in the presence of HIV Tat. Collectively, our results illustrate that an angiogenic repressive lncRNA, LINC00313, which is upregulated during KSHV reactivation, interacts with HIV Tat to promote endothelial cell motility. These results demonstrate that an lncRNA serves as a novel connector in HIV-KSHV interactions.
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