ArticleThe Journal of biological chemistry2010
Differential induction of interleukin-10 in monocytes by HIV-1 clade B and clade C Tat proteins.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Neurovirulent and non-neurovirulent strains of HIV-1 and their Tat proteins induce differential cytokine-chemokine profiles.NeuroImmune pharmacology and therapeutics · 2025Article
- The association between HIV-1 Tat and Vif amino acid sequence variation, inflammation and Trp-Kyn metabolism: an exploratory investigation.BMC infectious diseases · 2024Article
- Soluble CD14 is subtype-dependent in serum but not in cerebrospinal fluid in people with HIV.Journal of neuroimmunology · 2022Article
- Main lymphocyte subpopulations in cerebrospinal fluid and peripheral blood in HIV-1 subtypes C and B.Journal of neurovirology · 2022Article
- Short Communication: Genetic Variation in HumanAIDS research and human retroviruses · 2021Article
- The association of peripheral immune markers with brain cortical thickness and surface area in South African people living with HIV.Journal of neurovirology · 2020Article
- HIV-1 Tat - TLR4/MD2 interaction drives the expression of IDO-1 in monocytes derived dendritic cells through NF-κB dependent pathway.Scientific reports · 2020Article
- The Signature Amino Acid Residue Serine 31 of HIV-1C Tat Potentiates an Activated Phenotype in Endothelial Cells.Frontiers in immunology · 2020Article
- The Association of Immune Markers with Cognitive Performance in South African HIV-Positive Patients.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Article
- A Naturally Occurring Polymorphism in the HIV-1 Tat Basic Domain Inhibits Uptake by Bystander Cells and Leads to Reduced Neuroinflammation.Scientific reports · 2019Article
- The Evolving Profile of the Signature Amino Acid Residues in HIV-1 Subtype C Tat.AIDS research and human retroviruses · 2016Article
- Of mice and monkeys: can animal models be utilized to study neurological consequences of pediatric HIV-1 infection?ACS chemical neuroscience · 2015Review
- Article
- Anti-tat Hutat2:Fc mediated protection against tat-induced neurotoxicity and HIV-1 replication in human monocyte-derived macrophages.Journal of neuroinflammation · 2014Article
- Article
- Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND).AIDS research and therapy · 2014Review
- Article
- tat Exon 1 exhibits functional diversity during HIV-1 subtype C primary infection.Journal of virology · 2013Article
- HIV-1 Tat C modulates expression of miRNA-101 to suppress VE-cadherin in human brain microvascular endothelial cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The clade B human immunodeficiency virus, type 1 (HIV-1) Tat (trans-acting regulatory protein) induces interleukin-10 (IL-10) production in monocytes. IL-10, an anti-inflammatory cytokine, down-regulates proinflammatory cytokines and suppresses the immune response, leading to a rapid progression from HIV-1 infection to AIDS. Nine clades of HIV-1 are responsible for the majority of infections worldwide. Recent studies demonstrate that different HIV-1 clades have biological differences in relation to transmission, replication, and disease progression. In this study, we show that the cysteine to serine mutation at position 31, found in >90% of HIV-1 clade C Tat proteins, results in a marked decrease in IL-10 production in monocytes compared with clade B Tat. Additionally, the C31S mutation found in C Tat is responsible for the inability of these Tat proteins to produce high IL-10 levels in monocytes due to its inability to induce intracellular calcium flux through L-type calcium channels. Moreover, we show that p38alpha/p38beta and phosphoinositide 3-kinase are crucial to Tat-induced IL-10 production. These findings provide further evidence that HIV-1 clades differ in their biological properties that may impact HIV-1 pathogenesis and disease progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.