Influenza virus lectins display  diverse sugar-binding modes, but they share a feature–their sugar-binding sites are all located in cavities and are not easily  accessible to host antibodies and immune cells. As a comparison, the sugar-binding sites in host galectins are open  and easily  accessible.  It was thus hypothesized that these viral lectins all  originated from host galectins but have evolved to use hidden sugar-binding sites to evade host immune surveillance.