ArticleJournal of neurovirology2026
Role of extracellular vesicles derived from HIV-infected T cells and microglial cells in neuroinflammation and neuropathogenesis using a blood-brain barrier and cerebral organoid co-culture model.
Article in Journal of neurovirology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite effective antiretroviral therapy (ART) in suppressing HIV replication and reducing viral loads, latent reservoirs within the central nervous system (CNS) may contribute to persistent immune dysfunction, inflammation, and neurocognitive impairment in people living with HIV. Extracellular vesicles (EVs) isolated from serum and cerebrospinal fluid have been reported to contain HIV-1 RNAs, with their abundance associated with neurocognitive outcomes in ART-treated individuals. However, the mechanistic contribution of HIV-associated EVs in CNS pathology remains incompletely understood. In this study, we characterized EVs derived from latently HIV-1-infected T cells and microglial cells and identified HIV RNAs, including transactivation response element (TAR) RNA, Nef, and Tat RNA, within these particles. These EVs disrupted the integrity of a triple-cell blood–brain barrier (BBB) model by inducing apoptosis in BBB-associated cells. HIV-associated EVs were also able to traverse the BBB and promote apoptosis in cultured neuronal cells. In cerebral organoids derived from human induced pluripotent stem cells, these EVs induce production of pro-inflammatory cytokines, including IL-1β and TNF-α. Single-cell RNA sequencing of cerebral organoids exposed to microglial cell-derived EVs revealed upregulation of genes involved in double-stranded RNA signaling, apoptosis, inflammation, and microglial activation in response to HIV-associated EVs. Additionally, these EVs induced increased expression and phosphorylation of protein kinase R (PKR) in cerebral organoids. Plasma-derived EVs containing HIV RNA from individuals with HIV, but not control EVs from uninfected donors, induced apoptosis in both cerebral organoids and neuronal cells. These findings suggest that HIV-associated EVs may contribute to neuroinflammatory processes and cellular injury in CNS models, potentially informing mechanisms underlying HIV-related neurocognitive impairment that persist despite ART.
Indexed as
Identifiers
41866460What 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.