Many studies have shown that naked AgNPs have a good effect on the control and prevention of a variety of viral diseases (Table 1). However, the antiviral mechanism of nanosilver is still unclear. The antiviral action is associated with the following mechanisms: Nanosilver can prevent the virus from entering the host cells and inhibit the virus from binding to the cell receptor, thereby stopping the virus from infecting the targeted cells. AgNPs may be able to bind the viral surface protein and inhibit the interaction between the virus and the cell membrane receptors (Figure 2, left). However, it has been also reported that AgNPs can inactivate the virus through denaturation of surface proteins containing cysteine and methionine residues present on the viral capsid, in a similar way reported for bacteria. For example, AgNPs smaller than 10 nm were shown to interact with the sulfur-bearing residues of gp120 glycoprotein knobs distributed on the lipid membrane of HIV-1 virus, preventing the virus from binding to CD4 receptor site on the host cells, thus inhibiting the viral infection.11 By means of a viral adsorption assay, it was shown that the AgNP mechanism of anti-HIV action is based on the inhibition of the initial stages of the HIV-1 cycle. To demonstrate that the antiviral effect of AgNPs is due to the particle structure rather than to silver ions present in solution, the antiviral activity of silver sulfadiazine (AgSD) and silver nitrate (known antibacterial silver salts) was evaluated. Both salts showed a much lower therapeutic index than AgNPs in vitro, indicating that silver ions themselves are less efficient.12 These results point out that the antiviral efficacy is not only related to the dose of Ag+ ions present in solution but is also regulated by different other parameters (e.g., size, charge, and surface functionalization) associated with the nanosize dimension. For instance, in the case of Herpesviridae and Paramyxoviridae viruses (both enveloped viruses with embedded viral-encoded glycoproteins), AgNPs can effectively reduce their infectivity, by blocking the interaction between the viral particles and the host cells with an antiviral activity strictly dependent on the size and ζ potential of the AgNPs. As a general observation, it was reported that smaller nanoparticles have better antiviral effect. This effect was associated with the increase of the surface area, where smaller-sized AgNPs could bind more efficiently to the viral particles exerting a higher antiviral activity.13 Another study reported the impairment of Peste des petits ruminants virus (PPRV) replication after incubating infectious viral particles with AgNPs, which did not exhibit any virucidal effect even up to 900 μg/mL. This result suggested that the anti-PPRV activity of the AgNPs is due to the inhibitory effect on viral replication in the target cells. AgNPs do not prevent the binding of PPRV to host cells, but inhibit the entry of viruses into these cells. AgNPs can also interact with the surface and core of PPRV, but this interaction cannot kill the virus directly.12 The same results were then confirmed on other viruses. AgNPs with a diameter of 25 nm inhibited Vaccinia virus replication by preventing viral entry into host cells. However, AgNPs cannot prevent the virus from adsorbing onto the cells, and this virus is still infectious, indicating that AgNPs lack a direct virus-killing effect.13