Parsons and co‑authors demonstrate that rotavirus and norovirus replication depends on host fucosidase activity required for processing fucose‑containing glycans used by these viruses during infection. The work clarifies a common dependency across two major enteric pathogens and identifies host fucosidases as potential antiviral targets. Authors propose that small‑molecule or enzyme‑modulating approaches could disrupt viral entry or early replication steps without directly targeting viral proteins, reducing selective pressure for viral escape.