Compared to AgNPs, AuNPs exhibit reduced toxicity on healthy cells, making them more attractive for in vivo and clinical applications.38 Indeed, AuNPs have been successfully tested as inhibitors of viral entry into the host cells. AuNPs interact with hemagglutinin (HA), where Au is able to oxidize the disulfide bond of this glycoprotein causing its inactivation, thus impeding the membrane fusion of the virus with host cells. Targeting HA has emerged as an alternative strategy to the actual therapies (e.g., matrix protein 2 and neuramidase), especially to pandemic viruses that show an accelerated mutation speed of their surface proteins, hence a resistance to conventional treatments increasing their infectivity and mortality.38 This strategy has been applied to influenza (e.g., H1N1, HCV) and herpes viruses.39−44 The activity of AuNPs is proportional to the surface area exposed. As a consequence, the size and the morphology of these metal NPs play a substantial role in their antiviral activity. Recently, Kim et al. have reported that porous AuNPs are able to inhibit influenza A infection more efficiently than nonporous AuNPs.39 This effect has been associated with the higher surface area of the porous material that favors their interaction with capsids and thus increases their antiviral activity (Figure 4).