ArticleFrontiers in microbiology2016
Cocaine Enhances HIV-1 Transcription in Macrophages by Inducing p38 MAPK Phosphorylation.
Article in Frontiers in microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Investigation of exJSRV LTR promoter activity based on transcription factor regulatory networks.Frontiers in veterinary science · 2025Article
- The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in vitro.Journal of neurovirology · 2022Article
- Review
- Sophoridine Suppresses Herpes Simplex Virus Type 1 Infection by Blocking the Activation of Cellular PI3K/Akt and p38 MAPK Pathways.Frontiers in microbiology · 2022Article
- Drugs of Abuse and Their Impact on Viral Pathogenesis.Viruses · 2021Review
- Human Immunodeficiency Virus Type-1 (HIV-1) Transcriptional Regulation, Latency and Therapy in the Central Nervous System.Vaccines · 2021Review
- Interleukin-22 deficiency alleviates doxorubicin-induced oxidative stress and cardiac injury via the p38 MAPK/macrophage/Fizz3 axis in mice.Redox biology · 2020Article
- The impact of substance abuse on HIV-mediated neuropathogenesis in the current ART era.Brain research · 2019Review
- Article
- Synthetic Opioid Use and Common Injection-associated Viruses: Expanding the Translational Research Agenda.Current HIV research · 2019Review
- Substance use is independently associated with pneumonia severity in persons living with the human immunodeficiency virus (HIV).Substance abuse · 2019Article
- Baseline Cigarette Smoking Status as a Predictor of Virologic Suppression and CD4 Cell Count During One-Year Follow-Up in Substance Users with Uncontrolled HIV Infection.AIDS and behavior · 2018Article
- Cocaine evokes a profile of oxidative stress and impacts innate antiviral response pathways in astrocytes.Neuropharmacology · 2018Article
- HIV, Tat and dopamine transmission.Neurobiology of disease · 2017Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cocaine is a commonly used illicit drug among HIV-1 infected individuals and is known to increase HIV-1 replication in permissive cells including PBMCs, CD4(+) T cells, and macrophages. Cocaine's potentiating effects on HIV-1 replication in macrophages- the primary targets of the virus in the central nervous system, has been suggested to play an important role in HIV-1 neuro-pathogenesis. However, the mechanism by which cocaine enhances HIV-1 replication in macrophages remain poorly understood. Here, we report the identification of cocaine-induced signaling events that lead to enhanced HIV-1 transcription in macrophages. Treatment of physiologically relevant concentrations of cocaine enhanced HIV-1 transcription in a dose-dependent manner in infected THP-1 monocyte-derived macrophages (THP-1macs) and primary monocyte-derived macrophages (MDMs). Toward decoding the underlying mechanism, results presented in this report demonstrate that cocaine induces the phosphorylation of p38 mitogen activated protein kinase (p38 MAPK), a known activator of HIV-1 transcription. We also present data suggesting that the p38 MAPK-driven HIV-1 transcription is dependent on the induction of mitogen- and stress-activated protein kinase 1 (MSK1). Consequently, MSK1 mediates the phosphorylation of serine 10 residue of histone 3 (H3 Ser10), which is known to activate transcription of genes including that of HIV-1 in macrophages. Importantly, our results show that inhibition of p38 MAPK/MSK1 signaling by specific pharmacological inhibitors abrogated the positive effect of cocaine on HIV-1 transcription. These results validate the functional link between cocaine and p38 MAPK/MSK1 pathways. Together, our results demonstrate for the first time that the p38 MAPK/MSK1 signaling pathway plays a critical role in the cocaine-induced potentiating effects on HIV-1 infection, thus providing new insights into the interplay between cocaine abuse and HIV-1 neuro-pathogenesis.
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