Evidence map›Paper›PMID 39805095›Full record

ArticleASN neuro2025

Sex Affects Cognitive Outcomes in HIV-1 Tat Transgenic Mice: Role of CCR5.

Chloe A Simons, Sarah Kim, Yun K Hahn, Ama Boake-Agyei, Sara R Nass, Phu Vo, Kurt F Hauser, Pamela E Knapp

Abstract read
In one paragraph

Article in ASN neuro, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Chloe A SimonsDepartment of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
Sarah KimDepartment of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
Yun K HahnDepartment of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
Ama Boake-AgyeiDepartment of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
Sara R NassDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, Virginia, USA.
Phu VoDepartment of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
Kurt F HauserDepartment of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
Pamela E KnappDepartment of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.

Funding

MOR and CCR5 interactive signaling mediates opiate and HIV-driven synaptodendritic injuryR01DA034231 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI HAUSER, KURT F, KNAPP, PAMELA E · 2013 to 2023
$5.4M
pTau-related neuron and cognitive dysfunction in opioid-HIV comorbidity: Longitudinal and functional studiesR01DA060762 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI Kurt F Hauser, Pamela E Knapp · 2024 to 2026
$2.1M
NIDA NIH HHS R01 DA034231NIDA NIH HHS R01 DA060762
6 · The paper itself

Abstract

People living with HIV (PLWH) experience HIV-associated neurocognitive disorders (HAND), even though combination antiretroviral therapy (cART) suppresses HIV replication. HIV-1 transactivator of transcription (HIV-1 Tat) contributes to the development of HAND through neuroinflammatory and neurotoxic mechanisms. C-C chemokine 5 receptor (CCR5) is important in immune cell targeting and is a co-receptor for HIV viral entry into CD4+ cells. Notably, CCR5 has been implicated in cognition unrelated to HIV infection. Inhibition of CCR5 has been shown to improve learning and memory. To test whether CCR5 is involved in cognitive changes in HAND, we used a non-infectious, transgenic model in which HIV-1 Tat is inducibly expressed. Well-powered cohorts of male and female mice were placed on a diet containing doxycycline to induce Tat expression for 8-wks. Males showed Tat-mediated deficits in the Barnes maze test of spatial learning and memory; females showed no impairments. Deficits in the males were fully reversed by the CCR5 antagonist, maraviroc (MVC). Tat-mediated deficits were not found in novel object recognition or contextual fear conditioning in either sex. Based on earlier work, we hypothesized that MVC might increase brain-derived neurotrophic factor (BDNF), which is essential in maintaining synaptodendritic function. MVC did increase the mBDNF to proBDNF ratio in males, perhaps contributing to improved cognition.

Indexed as

CognitionReceptors, CCR5Sex Characteristicstat Gene Products, Human Immunodeficiency VirusAnimalsBrain-Derived Neurotrophic FactorCCR5 Receptor AntagonistsDisease Models, AnimalFearFemaleHIV-1MaleMaravirocMaze LearningMiceMice, Inbred C57BLBrain-Derived Neurotrophic FactorCCR5 protein, mouseCCR5 Receptor AntagonistsMaravirocReceptors, CCR5tat Gene Products, Human Immunodeficiency VirusBarnes mazeBDNFcontextual fear conditioninghippocampusmaraviroc (MVC)

Identifiers

PMID39805095
PMCPMC11877617

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Registered trials

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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.