ArticlePloS one2014
Immunopathogenesis of HIV infection in cocaine users: role of arachidonic acid.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Correlative Imaging to Detect Rare HIV Reservoirs and Associated Damage in Tissues.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Identification and Analysis of Differentially Expressed Genes Associated with Ferroptosis and HIV in PASMCs Based on Bioinformatics.Current HIV research · 2024Article
- Drugs of Abuse and Their Impact on Viral Pathogenesis.Viruses · 2021Review
- HIV-1 Tat and cocaine impact astrocytic energy reservoir influence on miRNA epigenetic regulation.Genomics · 2021Article
- HIV-1 Tat and cocaine impact mitochondrial epigenetics: effects on DNA methylation.Epigenetics · 2021Article
- Cocaine-mediated circadian reprogramming in the striatum through dopamine D2R and PPARγ activation.Nature communications · 2020Article
- Oxidative Stress in HIV Infection and Alcohol Use: Role of Redox Signals in Modulation of Lipid Rafts and ATP-Binding Cassette Transporters.Antioxidants & redox signaling · 2018Article
- Macrophages and Phospholipases at the Intersection between Inflammation and the Pathogenesis of HIV-1 Infection.International journal of molecular sciences · 2017Review
- Prostaglandin EFrontiers in physiology · 2017Review
- HIV and Cocaine Impact Glial Metabolism: Energy Sensor AMP-activated protein kinase Role in Mitochondrial Biogenesis and Epigenetic Remodeling.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Arachidonic acid (AA) is known to be increased in HIV infected patients and illicit drug users are linked with severity of viral replication, disease progression, and impaired immune functions. Studies have shown that cocaine accelerates HIV infection and disease progression mediated by immune cells. Dendritic cells (DC) are the first line of antigen presentation and defense against immune dysfunction. However, the role of cocaine use in HIV associated acceleration of AA secretion and its metabolites on immature dendritic cells (IDC) has not been elucidated yet. The aim of this study is to elucidate the mechanism of AA metabolites cyclooxygenase-2 (COX-2), prostaglandin E2 synthetase (PGE2), thromboxane A2 receptor (TBXA2R), cyclopentenone prostaglandins (CyPG), such as 15-deoxy-Δ12,14-PGJ2 (15d-PGJ2), 14-3-3 ζ/δ and 5-lipoxygenase (5-LOX) mediated induction of IDC immune dysfunctions in cocaine using HIV positive patients. The plasma levels of AA, PGE2, 15d-PGJ2, 14-3-3 ζ/δ and IDC intracellular COX-2 and 5-LOX expression were assessed in cocaine users, HIV positive patients, HIV positive cocaine users and normal subjects. Results showed that plasma concentration levels of AA, PGE2 and COX-2, TBXA2R and 5-LOX in IDCs of HIV positive cocaine users were significantly higher whereas 15d-PGJ2 and 14-3-3 ζ/δ were significantly reduced compared to either HIV positive subjects or cocaine users alone. This report demonstrates that AA metabolites are capable of mediating the accelerative effects of cocaine on HIV infection and disease progression.
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Registered trials
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