SNX17 facilitates entry and infection of Rift Valley fever virus and related bunyaviruses.

SNX17 is essential for efficient Rift Valley fever virus infection, with its removal causing a substantial reduction in infection rates in knockout cells.

• Why it matters: Understanding host factors like SNX17 can reveal new targets for antiviral strategies against bunyaviruses, which include pathogens like RVFV that cause human outbreaks.
• What they did: Researchers characterized SNX17's role by analyzing its interaction with RVFV and other bunyaviruses, finding that knockout of SNX17 reduces infection and that SNX17 interacts with RVFV Gc and co-migrates with the virus to late endosomes.
• The result: The findings suggest SNX17 plays a broader role in bunyaviral entry, enabling further exploration of host-targeted interventions for bunyavirus infections.