Researchers discovered that both rotavirus and norovirus replication depend on host fucosidase activity, revealing a conserved glycan-processing vulnerability in two major gastrointestinal pathogens. The study used genetic and pharmacologic loss-of-function approaches to show fucose cleavage is required for viral entry or uncoating steps. Authors propose fucosidase inhibition as a host-directed antiviral strategy that could reduce resistance risk. Fucosidase enzymes remove fucose residues from glycoconjugates; targeting host enzymatic processes offers a broad-spectrum approach but requires careful safety evaluation given glycan roles in host physiology.