Polysaccharides, especially sulfated polysaccharides, can interact with the surface of virus by negative charge, thereby inhibiting the infectious ability of the virus, or killing the virus directly. Pathogens use GAGs at almost every major entry portal to promote their attachment and invasion of host cells, to move from one cell to another, and to protect themselves from immune attack [22]. For example, fucosylated chondroitin sulfate was effective in blocking laboratory strain HIV-1IIIB entry and replication (4.26 μg/mL and 0.73 μg/mL, respectively), and inhibiting infection by clinic isolate HIV-1KM018 and HIV-1TC-2 (23.75 μg/mL and 31.86 μg/mL, respectively) as well as suppressing HIV-1 drug-resistant virus. Further studies indicated that fucosylated chondroitin sulfate can potently bind the recombinant HIV-1 gp120 protein to inhibit several strains of HIV-1 [82]. A cationically modified chitosan derivative, HTCC, has been shown to be an effective inhibitor of HCoV-NL63 replication. The analysis of the interaction between HTCC polymer and the recombinant ectodomain of the S protein from CoV showed binding, resulting in the formation of protein-polymer complexes. One may assume that such binding will result in the efficient inactivation of the virus [83]. Carrageenan acts primarily by preventing the binding or the entry of virions into cells [84,85]. Iota-carrageenan, a high molecular weight sulfated polysaccharide, is an approved antiviral drug that interacts with the viral surface [67]. The binding and inactivation of virus particles by iota-carrageenan are fast and highly effective. During the residence time of the iota-carrageenan containing lozenge in the mouth, the viral titer is reduced by 85% and 91% for IAV and HCoV-OC43, respectively [67]. Furthermore, animal experiments have shown that iota-carrageenan can reduce the spreading of influenza virus in surface epithelia of infected animals, and thereby provided sufficient benefits for animals to promote survival [86].