Latent HIV-1 reservoirs remain a central obstacle to a functional cure because the virus can persist silently in infected cells despite antiretroviral therapy. “Shock-and-kill” strategies aim to reactivate (“shock”) latent virus so infected cells become visible to immune clearance or additional therapies, but clinically safe and effective latency-reversing approaches are still limited.
In this study, researchers investigated whether exosomes could mediate latency reversal after exposure to Astragalus polysaccharide (APS). Using the HIV-1 latency model J-Lat Full Length 10.6, they generated exosomes from APS-treated reservoir cells (APS-Lat-EXO) and compared them with exosomes from untreated cells (Lat-EXO). When applied to recipient cells, APS-Lat-EXO significantly enhanced HIV-1 reactivation, assessed by increased GFP⁺ proportions (flow cytometry), elevated p24 levels (ELISA), and upregulated Gag/LTR transcripts (RT-qPCR). Similar reactivation signals were also observed in PBMCs from HIV-1-infected individuals.
Proteomic and miRNA profiling revealed distinct exosomal cargo after APS exposure, with enrichment pointing to PI3K/AKT and links to NF-κB regulation. Western blot validation supported activation of the PI3K/AKT/NF-κB axis, consistent with transcriptional reawakening of latent HIV-1. These findings highlight APS-Lat-EXO as a bio-derived, mechanistically defined candidate to support latency-reversal research within the shock-and-kill framework.
The work titled “ Astragalus polysaccharide promotes latent HIV-1 reactivation via exosome-mediated modulation of the PI3K/AKT/NF-κB axis ”, was published on Extracellular Vesicles and Circulating Nucleic Acids (published on January 29, 2026).
Extracellular Vesicles and Circulating Nucleic Acids
Experimental study
Not applicable
Astragalus polysaccharide promotes latent HIV-1 reactivation via exosome-mediated modulation of the PI3K/AKT/NF-κB axis
29-Jan-2026