ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009
CXCR3 activation by lentivirus infection suppresses neuronal autophagy: neuroprotective effects of antiretroviral therapy.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Brain microbial populations in HIV/AIDS: α-proteobacteria predominate independent of host immune status.PloS one · 2013Trial
- Combination Antiretroviral Therapy and Immunophenotype of Feline Immunodeficiency Virus.Viruses · 2023Article
- Article
- A Rationale and Approach to the Development of Specific Treatments for HIV Associated Neurocognitive Impairment.Microorganisms · 2022Review
- Role of CXCL10 in Spinal Cord Injury.International journal of medical sciences · 2022Review
- Matrix metalloproteinases in the CNS: interferons get nervous.Cellular and molecular life sciences : CMLS · 2019Review
- Neurologic disease in feline immunodeficiency virus infection: disease mechanisms and therapeutic interventions for NeuroAIDS.Journal of neurovirology · 2018Review
- Inflammasome induction in Rasmussen's encephalitis: cortical and associated white matter pathogenesis.Journal of neuroinflammation · 2013Article
- Differential type 1 interferon-regulated gene expression in the brain during AIDS: interactions with viral diversity and neurovirulence.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Programming of neurotoxic cofactor CXCL-10 in HIV-1-associated dementia: abrogation of CXCL-10-induced neuro-glial toxicity in vitro by PKC activator.Journal of neuroinflammation · 2012Article
- Role of endolysosomes in HIV-1 Tat-induced neurotoxicity.ASN neuro · 2012Article
- Delineating HIV-associated neurocognitive disorders using transgenic models: the neuropathogenic actions of Vpr.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012Review
- Dual role of autophagy in HIV-1 replication and pathogenesis.AIDS research and therapy · 2012Article
- Article
- Proteinase-activated receptor-1 mediates dorsal root ganglion neuronal degeneration in HIV/AIDS.Brain : a journal of neurology · 2011Article
- Impaired neurosteroid synthesis in multiple sclerosis.Brain : a journal of neurology · 2011Article
- Inflammation and epithelial cell injury in AIDS enteropathy: involvement of endoplasmic reticulum stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Interactions between human immunodeficiency virus (HIV)-1 Vpr expression and innate immunity influence neurovirulence.Retrovirology · 2011Article
- Age- and disease-dependent HERV-W envelope allelic variation in brain: association with neuroimmune gene expression.PloS one · 2011Article
- Hepatitis C virus core protein induces neuroimmune activation and potentiates Human Immunodeficiency Virus-1 neurotoxicity.PloS one · 2010Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Previous studies have implicated CXCL12 in the neuropathogenesis of HIV infection. Proteolysis of CXCL12 generates a neurotoxic molecule, CXCL12(5-67), which engages and activates CXCR3, in addition to exhibiting increased expression in the brains of patients with HIV-associated dementia (HAD). Herein, we investigated CXCR3-mediated neuronal injury, particularly, its contribution to autophagy suppression and the concomitant effects of antiretroviral therapy using human brain samples and models of HIV neuropathogenesis. Neurons in the brains of HAD patients and feline immunodeficiency virus (FIV)-infected animals, as well as cultured human neurons, expressed CXCR3, which was modulated in a ligand-specific manner. Exposure of human neurons to CXCL12(5-67) caused a reduction in the autophagy-associated molecule LC3 (P<0.05) and neuronal survival (P<0.05), which recapitulated findings in FIV- and HIV-infected brains (P<0.05). Oral didanosine (ddI) treatment of FIV-infected animals reduced neurobehavioral abnormalities in conjunction with diminished plasma viral load (P<0.05). F4/80 transcript abundance and CXCL12(5-67) immunoreactivity were reduced with restored neuronal LC3 expression in the brains of FIV-infected animals after ddI treatment (P<0.05). ddI treatment also prevented microglial activation and depletion of synaptic proteins in the cortex of FIV-infected animals (P<0.05). These findings indicate that the beneficial effects of ddI might be a consequence of a reduced systemic viral burden and concurrent leukocyte activation, leading to diminished neuroinflammation with preservation of neuronal autophagy by regulating CXCR3 activation.
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