Lei Lu¹, Raymond WY Sun², Chee-Kin Hui³, Rong Chen², John M Luk⁴, Chi M Che², George KK Lau¹

¹ Department of Medicine, The University of Hong Kong, ² Department of Chemsitry, The University of Hong Kong, ³ Department of Microbiology, The University of Hong Kong, ⁴ Department of Surgery, The University of Hong Kong

Introduction : Silver nanoparticles could inhibit the in vitro production of HBV RNA and extracellular virions. The objective of the present study was to investigate the anti-HBV mechanism of silver nanoparticles.

Methods : The interactions between silver nanoparticles and HBV DNA were determined by gel mobility shift assay and absorption titration assay. Using the HepAD38 cell line as the in vitro infection model, the binding activities between HBV viral particles and silver nanoparticles were revealed by transmission electronic microscopy, and the binding affinity was further determined in a co-incubation model by real time PCR.

Results : Our results revealed that silver nanoparticles (Ag10Ns and Ag50Ns) were able to inhibit the formation of intracellular HBV RNA and reduce the extracellular HBV DNA formation of HepAD38 cells by over 50% compared to the vehicle control. Gel mobility shift assay indicated that Ag10Ns could bind to HBV dsDNA at 1:50 DNA to silver molar ratio, and the absorption titration assay revealed that silver nanoparticles had good binding affinity to HBV DNA with the binding constant (Kb) of (8.8 ± 1.0) × 10⁵ dm³mol^-1. Ag10Ns also showed good binding affinity to HBV virions, as only 54% and 12% unbounded viral particles (vs silver-nanoparticle-free control) were detected after co-incubation with coated Ag10Ns for 10 and 60 min, respectively.

Conclusions : Silver nanoparticles could directly interact with both HBV dsDNA and viral particles, and they may exert the anti-HBV activities through this binding-based mechanism.

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