Abstract
BackgroundSilver nanoparticles have proven to exert antiviral activity against HIV-1 at non-cytotoxic concentrations, but the mechanism underlying their HIV-inhibitory activity has not been not fully elucidated. In this study, silver nanoparticles are evaluated to elucidate their mode of antiviral action against HIV-1 using a panel of different in vitro assays.ResultsOur data suggest that silver nanoparticles exert anti-HIV activity at an early stage of viral replication, most likely as a virucidal agent or as an inhibitor of viral entry. Silver nanoparticles bind to gp120 in a manner that prevents CD4-dependent virion binding, fusion, and infectivity, acting as an effective virucidal agent against cell-free virus (laboratory strains, clinical isolates, T and M tropic strains, and resistant strains) and cell-associated virus. Besides, silver nanoparticles inhibit post-entry stages of the HIV-1 life cycle.ConclusionsThese properties make them a broad-spectrum agent not prone to inducing resistance that could be used preventively against a wide variety of circulating HIV-1 strains.
Highlights
Silver nanoparticles have proven to exert antiviral activity against HIV-1 at non-cytotoxic concentrations, but the mechanism underlying their HIV-inhibitory activity has not been not fully elucidated
By means of a luciferase-based assay, the 50% cytotoxic concentration (CC50) of silver nanoparticles was defined as 3.9 ± 1.6 mg/mL against HeLa-CD4-LTR-b-gal cells, as 1.11 ± 0.32 mg/mL against human Peripheral blood mononuclear cells (PBMC), and 1.3 ± 0.58 mg/mL against MT-2 cells
Range of antiviral activity Silver nanoparticles of 30-50 nm were tested against a panel of HIV-1 isolates using indicator cells in which infection was quantified by a luciferase-based assay
Summary
Silver nanoparticles have proven to exert antiviral activity against HIV-1 at non-cytotoxic concentrations, but the mechanism underlying their HIV-inhibitory activity has not been not fully elucidated. Silver nanoparticles are evaluated to elucidate their mode of antiviral action against HIV-1 using a panel of different in vitro assays. Studies have shown that 5%-78% of treated patients receiving antiretroviral therapy are infected with HIV-1 viruses that are resistant to at least one of the available drugs [2]. For these reasons, there is a need for new anti-HIV agents that function over viral stages other than retrotranscription or protease activity and that can be used for treatment and prevention of HIV/AIDS dissemination [3]. Fusion or entry inhibitors are considered an attractive option, since blocking HIV entry into its target cell leads to suppression of viral infectivity, replication, and the cytotoxicity induced by the virus-cell interaction [4]
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