Authors
Sarah Schmidlin, Oandy Naranjo, Silvia Torices, Nikolai Fattakhov, Monika Gilicinska, Masha Minevich, Kyra Schindler, Destiny Tiburcio, Olivia Osborne, Arpan Acharya, Minseon Park, Mario Stevenson, Siddappa Byrareddy, Michal Toborek
Published in
Research square. Aug 12, 2026. Epub Aug 12, 2026.
Abstract
HIV-Associated Neurocognitive Impairments persist, with over 50% of patients experiencing cognitive decline. Blood-brain barrier (BBB) impairment is a consistent feature of this comorbidity, which is remarkable, because BBB endothelial cells are not productively infected by HIV-1. Conversely, pericytes can be productively infected with HIV-1 and are essential for cerebrovascular homeostasis. Given this, we hypothesized that HIV-1 infection of pericytes disrupts BBB endothelial cell integrity through dysfunctional gap junction and hemichannel signaling, impairing pericyte-endothelial intercellular communication. Using a co-culture model with primary human BBB pericytes and brain microvascular endothelial cells, pericytes were infected with HIV-1 for 3 or 7 days, exhibiting active and latent viral phenotypes. Findings revealed enhanced gap junction communication between HIV-infected pericytes and endothelial cells under both conditions, and blocking gap junctions modulated endothelial inflammatory responses. Overall, this study advances our understanding of the molecular mechanisms underlying HIV-associated BBB dysfunction and may inform the development of targeted therapeutic strategies.
PMID:
42845645
Bibliographic data and abstract were imported from PubMed on 08 Oct 2026.
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