Review uncovers extracellular vesicle mechanisms driving viral persistence and immune dysregulation in HIV infection, highlighting novel therapeutic delivery and gene-editing platforms.
Key Points
To review the molecular mechanisms by which extracellular vesicles mediate HIV pathogenesis, viral latency, and immune dysregulation, and to assess their utility as therapeutic targets and delivery vehicles.
Narrative synthesis of molecular and clinical literature examining extracellular vesicle biogenesis, composition, and host-pathogen interactions during HIV infection.
Analysis of mechanistic pathways linking extracellular vesicles to viral dissemination, latent reservoir maintenance, and chronic inflammatory states.
Evaluation of bioengineering approaches employing modified vesicles for targeted drug delivery, gene editing, and immunomodulatory interventions.
Extracellular vesicles act as key intermediaries in HIV pathogenesis by transferring viral proteins and regulatory RNAs that facilitate viral dissemination and sustain latent reservoirs.
Vesicle signaling exerts divergent immunological effects, driving chronic systemic inflammation and immune exhaustion while blunting host antiviral defenses.
Engineered extracellular vesicles demonstrate significant therapeutic potential as biocompatible delivery systems for antiretrovirals, gene-editing machinery, and targeted immunotherapies.