ArticleFree radical biology & medicine2014
Immunoneuropathogenesis of HIV-1 clades B and C: role of redox expression and thiol modification.
Article in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Glutathione in HIV-Associated Neurocognitive Disorders.Current issues in molecular biology · 2024Review
- Article
- HIV-Tat and Cocaine Impact Brain Energy Metabolism: Redox Modification and Mitochondrial Biogenesis Influence NRF Transcription-Mediated Neurodegeneration.Molecular neurobiology · 2021Article
- 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
- Characterization of Nanodiamond-based anti-HIV drug Delivery to the Brain.Scientific reports · 2018Article
- Conditional Human Immunodeficiency Virus Transactivator of Transcription Protein Expression Induces Depression-like Effects and Oxidative Stress.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2017Article
- Deficiency in DNA damage response, a new characteristic of cells infected with latent HIV-1.Cell cycle (Georgetown, Tex.) · 2017Article
- HIV and Cocaine Impact Glial Metabolism: Energy Sensor AMP-activated protein kinase Role in Mitochondrial Biogenesis and Epigenetic Remodeling.Scientific reports · 2016Article
- Effects of Cigarette Smoke Condensate on Oxidative Stress, Apoptotic Cell Death, and HIV Replication in Human Monocytic Cells.PloS one · 2016Article
- HIV Subtypes B and C gp120 and Methamphetamine Interaction: Dopaminergic System Implicates Differential Neuronal Toxicity.Scientific reports · 2015Article
- HIV-1, methamphetamine and astrocytes at neuroinflammatory Crossroads.Frontiers in microbiology · 2015Review
- Synaptic Plasticity and Neurological Disorders in Neurotropic Viral Infections.Neural plasticity · 2015Review
- Drugs of Abuse in HIV infection and neurotoxicity.Frontiers in microbiology · 2015Article
- Vorinostat positively regulates synaptic plasticity genes expression and spine density in HIV infected neurons: role of nicotine in progression of HIV-associated neurocognitive disorder.Molecular brain · 2014Article
- HIV-1 subtypes B and C Tat differentially impact synaptic plasticity expression and implicates HIV-associated neurocognitive disorders.Current HIV research · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
Previous studies have shown that, during infection, HIV-1 clade B and clade C differentially contribute to the neuropathogenesis and development of HIV-associated neurocognitive disorders (HANDs). The low-molecular-weight tripeptide glutathione (GSH) alters the redox balance and leads to the generation of reactive oxygen species, which play a significant role in the neuropathogenesis of HANDs. We hypothesized that the HIV-1 clade B and clade C viruses and their respective Tat proteins exert differential effects on monocyte-derived immature dendritic cells (IDCs) and neuroblastoma cells (SK-N-MC) by redox activation, which leads to immunoneuropathogenesis. The GSH/GSSG ratio and mRNA expression levels and protein modification of glutathione synthetase (GSS), glutathione peroxidase 1 (GPx1), superoxide dismutase 1 (SOD1), and catalase (CAT) were analyzed in IDCs infected with HIV-1 clade B or clade C as well as in cells treated with the respective Tat proteins. The results indicated that HIV-1 clade B virus and its Tat protein significantly increased the production of reactive oxygen species and reduced the GSH/GSSG ratio and subsequent downregulation of gene expression and protein modification of GSS, GPx1, SOD1, and CAT compared to infection with the clade C virus or treatment with the clade C Tat protein. Thus, our studies demonstrate that HIV-1 clades B and C exert differential effects of redox expression and thiol modification. HIV-1 clade B potentially induces oxidative stress, leading to more immunoneuropathogenesis than infection with HIV-1 clade C.
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