ArticleFrontiers in microbiology2015
The dual action of poly(ADP-ribose) polymerase -1 (PARP-1) inhibition in HIV-1 infection: HIV-1 LTR inhibition and diminution in Rho GTPase activity.
Article in Frontiers in microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- NADThe Journal of general virology · 2026Review
- Bloom syndrome helicase is required for efficient HIV-1 reverse transcription in macrophages.bioRxiv : the preprint server for biology · 2026Article
- PARPs and PARP inhibitors: molecular mechanisms and clinical applications.Molecular biomedicine · 2025Review
- Decoding NAD+ Metabolism in COVID-19: Implications for Immune Modulation and Therapy.Vaccines · 2024Review
- Review
- NAD+-consuming enzymes in immune defense against viral infection.The Biochemical journal · 2021Review
- Noncytotoxic functions of killer cell granzymes in viral infections.PLoS pathogens · 2021Review
- Brain tissue transcriptomic analysis of SIV-infected macaques identifies several altered metabolic pathways linked to neuropathogenesis and poly (ADP-ribose) polymerases (PARPs) as potential therapeutic targets.Journal of neurovirology · 2021Article
- Virus-Host Interplay Between Poly (ADP-Ribose) Polymerase 1 and Oncogenic Gammaherpesviruses.Frontiers in microbiology · 2021Review
- Kaposi's sarcoma-associated herpesvirus processivity factor (PF-8) recruits cellular E3 ubiquitin ligase CHFR to promote PARP1 degradation and lytic replication.PLoS pathogens · 2021Article
- NADFrontiers in molecular biosciences · 2021Review
- Poly(ADP-Ribose) Polymerase Inhibition in Acute Lung Injury. A Reemerging Concept.American journal of respiratory cell and molecular biology · 2020Review
- Review
- Electronic cigarette exposure disrupts blood-brain barrier integrity and promotes neuroinflammation.Brain, behavior, and immunity · 2020Article
- Combination of HIV-1 and Diabetes Enhances Blood Brain Barrier Injury via Effects on Brain Endothelium and Pericytes.International journal of molecular sciences · 2020Article
- Human immunodeficiency virus type 1 transcription is regulated by thieno[3,4-Experimental and therapeutic medicine · 2020Article
- Diverse therapeutic efficacies and more diverse mechanisms of nicotinamide.Metabolomics : Official journal of the Metabolomic Society · 2019Review
- Article
- The PARP1-Siah1 Axis Controls HIV-1 Transcription and Expression of Siah1 Substrates.Cell reports · 2018Article
- PARP inhibition in leukocytes diminishes inflammation via effects on integrins/cytoskeleton and protects the blood-brain barrier.Journal of neuroinflammation · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Multifactorial mechanisms comprising countless cellular factors and virus-encoded transactivators regulate the transcription of HIV-1 (HIV). Since poly(ADP-ribose) polymerase 1 (PARP-1) regulates numerous genes through its interaction with various transcription factors, inhibition of PARP-1 has surfaced recently as a powerful anti-inflammatory tool. We suggest a novel tactic to diminish HIV replication via PARP-1 inhibition in an in vitro model system, exploiting human primary monocyte-derived macrophages (MDM). PARP-1 inhibition was capable to lessen HIV replication in MDM by 60-80% after 7 days infection. Tat, tumor necrosis factor α (TNFα), and phorbol 12-myristate 13-acetate (PMA) are known triggers of the Long Terminal Repeat (LTR), which can switch virus replication. Tat overexpression in MDM transfected with an LTR reporter plasmid resulted in a 4.2-fold increase in LTR activation; PARP inhibition caused 70% reduction of LTR activity. LTR activity, which increased 3-fold after PMA or TNFα treatment, was reduced by PARP inhibition (by 85-95%). PARP inhibition in MDM exhibited 90% diminution in NFκB activity (known to mediate TNFα- and PMA-induced HIV LTR activation). Cytoskeleton rearrangements are important in effective HIV-1 infection. PARP inactivation reduced actin cytoskeleton rearrangements by affecting Rho GTPase machinery. These discoveries suggest that inactivation of PARP suppresses HIV replication in MDM by via attenuation of LTR activation, NFκB suppression and its effects on the cytoskeleton. PARP appears to be essential for HIV replication and its inhibition may provide an effective approach to management of HIV infection.
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