ArticleAIDS research and human retroviruses2011
Differential induction of rat neuronal excitotoxic cell death by human immunodeficiency virus type 1 clade B and C tat proteins.
Article in AIDS research and human retroviruses, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- Autophagy induction by histone deacetylase inhibitors inhibits HIV type 1.The Journal of biological chemistry · 2015Trial
- HIV gp120 induces TREM1 expression through TLR-PGE₂ signalling in human monocyte-derived microglia.Journal of neuroinflammation · 2026Article
- A pilot investigation of the association between HIV-1 Vpr amino acid sequence diversity and the tryptophan-kynurenine pathway as a potential mechanism for neurocognitive impairment.Virology journal · 2024Article
- HIV-1 Tat Upregulates TREM1 Expression in Human Microglia.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Reduced neuronal population in the dorsolateral prefrontal cortex in infant macaques infected with simian immunodeficiency virus (SIV).Journal of neurovirology · 2021Article
- Opioid and neuroHIV Comorbidity - Current and Future Perspectives.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Review
- SMAC mimetics induce autophagy-dependent apoptosis of HIV-1-infected macrophages.Cell death & disease · 2020Article
- Article
- Differential Contribution of HIV-1 Subtypes B and C to Neurological Disorders: Mechanisms and Possible Treatments.AIDS reviews · 2019Review
- SMAC Mimetics Induce Autophagy-Dependent Apoptosis of HIV-1-Infected Resting Memory CD4+ T Cells.Cell host & microbe · 2018Article
- Induction of autophagy by PI3K/MTOR and PI3K/MTOR/BRD4 inhibitors suppresses HIV-1 replication.The Journal of biological chemistry · 2018Article
- Multivariable analysis to determine if HIV-1 Tat dicysteine motif is associated with neurodevelopmental delay in HIV-infected children in Malawi.Behavioral and brain functions : BBF · 2015Article
- Of mice and monkeys: can animal models be utilized to study neurological consequences of pediatric HIV-1 infection?ACS chemical neuroscience · 2015Review
- Effect of HIV clade differences on the onset and severity of HIV-associated neurocognitive disorders.Journal of neurovirology · 2013Review
- HIV clades B and C are associated with reduced brain volumetrics.Journal of neurovirology · 2013Article
- HIV-1 Tat protein variants: critical role for the cysteine region in synaptodendritic injury.Experimental neurology · 2013Article
- Effects of Tat proteins and Tat mutants of different human immunodeficiency virus type 1 clades on glial JC virus early and late gene transcription.The Journal of general virology · 2013Article
- Neuronal toxicity in HIV CNS disease.Future virology · 2012Article
- The Impact of HIV Coinfection on Cerebral Malaria Pathogenesis.Journal of neuroparasitology · 2012Article
- Article
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4 authors at 3 institutions in 1 country.
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Abstract
In the absence of effective antiretroviral therapy, infection with clade B human immunodeficiency virus (HIV-1) infection commonly progresses to AIDS dementia. However, in India, where clade C infection is most prevalent, severe cognitive impairment due to HIV-1 is reported to be less prevalent. The Tat protein of HIV-1, which is released from HIV-1-infected macrophages, is thought to play a major role in the disruption of neuronal function as well as in the infiltration of macrophages associated with advanced neuropathogenesis. Clade B Tat is excitotoxic to hippocampal neurons by potentiating N-methyl-d-aspartate-induced currents of the zinc-sensitive NR1/NR2A N-methyl-d-aspartate receptor in a zinc-binding-dependent mechanism. This study characterizes the zinc-binding properties of clade C Tat protein. Using ultraviolet spectroscopy and the Ellman reaction, we show that clade C Tat protein binds just one zinc ion per monomer. We then investigated the ability of clade C Tat to block the inhibition of N-methyl-d-aspartate receptors from zinc antagonism through ion chelation. Although clade C Tat enhanced N-methyl-d-aspartate-mediated rat hippocampus neuronal toxicity in the presence of zinc, the increase was significantly less than that observed with clade B Tat. These findings suggest that the observed differences in neuropathogenesis found with HIV-1 clade C infection compared to clade B may, in part, be due to a decrease in Tat-mediated neurotoxicity.
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