ArticlebioRxiv : the preprint server for biology2025
HIV infection in microglia leads to senescence, triggering activation of neurotoxicity pathways.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- HIV-1 Tat and gp120 as key drivers of neurodegeneration in the central nervous system.Frontiers in microbiology · 2026Review
- The prefrontal cortex as a target of HIV-1 neurotoxicity: molecular mechanisms of viral protein-mediated neurodegeneration and executive dysfunction.Frontiers in cellular neuroscience · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
HIV-associated neurocognitive disorders (HAND) persist in milder forms despite anti-retroviral therapy, leading to premature and exacerbated aging-related cognitive disorders. We investigated the interplay between HAND and aging in microglia, which constitute the main brain HIV reservoir. We compared the transcriptomic patterns associated with normal aging in healthy humans to those observed following HIV infection in both ex vivo and in vivo models. Single cell and bulk transcriptomic patterns revealed that HIV infection induces a pattern of cellular senescence, with strong parallels to the transcriptomic signature of normal aging. Both processes were characterized by p53 pathway activation, upregulation of inflammatory genes and downregulation of proliferative genes while maintaining mTOR signaling, a pattern characteristic of cellular senescence. Importantly, both actively HIV infected and bystander microglia showed the cellular senescence patterns. Our results provide a mechanistic basis for the observed premature brain aging in HAND, and identify senescence-associated pathways as potential therapeutic targets.
Indexed as
Identifiers
What OpenQuestion holds
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.