ArticleNeurotoxicity research2011
HIV-1 clade B and C isolates exhibit differential replication: relevance to macrophage-mediated neurotoxicity.
Article in Neurotoxicity research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- HIV-1 Tat: Role in Bystander Toxicity.Frontiers in cellular and infection microbiology · 2020Review
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- Small molecule ONC201 inhibits HIV-1 replication in macrophages via FOXO3a and TRAIL.Antiviral research · 2019Article
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- HIV/neuroAIDS biomarkers.Progress in neurobiology · 2017Review
- HIV-1 Gp120 clade B/C induces a GRP78 driven cytoprotective mechanism in astrocytoma.Oncotarget · 2017Article
- Neuroimaging abnormalities in clade C HIV are independent of Tat genetic diversity.Journal of neurovirology · 2017Article
- Article
- Glutaminase-containing microvesicles from HIV-1-infected macrophages and immune-activated microglia induce neurotoxicity.Molecular neurodegeneration · 2015Article
- Envelope gene evolution and HIV-1 neuropathogenesis.Journal of neuroinfectious diseases · 2015Article
- Impact of the HIV Tat C30C31S dicysteine substitution on neuropsychological function in patients with clade C disease.Journal of neurovirology · 2014Article
- HIV clades B and C are associated with reduced brain volumetrics.Journal of neurovirology · 2013Article
- IL-1β and TNF-α induce neurotoxicity through glutamate production: a potential role for neuronal glutaminase.Journal of neurochemistry · 2013Article
- Article
- STAT1 regulates human glutaminase 1 promoter activity through multiple binding sites in HIV-1 infected macrophages.PloS one · 2013Article
- Human immunodeficiency virus type 1 (HIV-1) transactivator of transcription through its intact core and cysteine-rich domains inhibits Wnt/β-catenin signaling in astrocytes: relevance to HIV neuropathogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Neuroimaging markers of human immunodeficiency virus infection in South Africa.Journal of neurovirology · 2012Article
- Platelet-derived growth factor CC-mediated neuroprotection against HIV Tat involves TRPC-mediated inactivation of GSK 3beta.PloS one · 2012Article
- Article
- Interferon-α regulates glutaminase 1 promoter through STAT1 phosphorylation: relevance to HIV-1 associated neurocognitive disorders.PloS one · 2012Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
HIV-associated neurocognitive disorders (HAND) continue to be a consequence of HIV-1 infection among clade B-infected individuals. In contrast, the incidence of severe neurological impairment is lower among clade C-infected patients in regions of Sub-Saharan Africa and India. Biological aspects such as replication, cytopathicity, inflammatory response, and neurotoxicity unique to each clade influence neuropathogenicity and ultimately affect the clinical outcome of the disease. We hypothesize that productive infection by clade C isolates leads to macrophage-mediated neurotoxicity, although to a lesser extent than clade B isolates. Using a panel of primary isolates of clades B and C we demonstrated that clade B has higher replication efficiency in monocyte-derived macrophages (MDM) through reverse transcriptase activity assay and HIV-1 p24 antigen ELISA. To test the neurotoxicity of clades B and C, we used an in vitro neurotoxicity model. Conditioned medium from clade B-infected MDM was neurotoxic to rat and human neuron cultures. In contrast, clade C isolates mediated neurotoxicity when a higher initial viral titer was used for MDM infection. Furthermore, neurotoxicity mediated by isolates of both clades correlated with virus replication in MDM. Together, these results suggest that in comparison to clade B, primary isolates of clade C have slower replication kinetics in primary MDM, leading to lower levels of macrophage-mediated neurotoxicity. Elucidating the differences in replication and macrophage-mediated neurotoxicity between isolates of HIV-1 clades B and C will provide important insights needed to clarify the disparity seen in HAND incidence.
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