Avian reovirus triggered ferroptosis, modulated lipid metabolism, and induced lipid droplet formation in infected cells, which was mediated in part by the p10/FAST protein

Avian reovirus infection of chicken LMH cells increases lipid droplet size and number and triggers ferroptosis, with oxidative stress and lipid peroxidation that are partially iron dependent.

• Why it matters: Viral replication can reshape host lipid handling, but how avian reovirus alters membrane vulnerability and cell-death pathways to support spread is unclear.
• What they did: ARV-infected LMH cells were profiled by lipidomics and transcriptomics, then ferroptosis was tested via oxidative stress/lipid peroxidation readouts and iron dependence; p10/FAST transfection was used to model syncytia.
• The result: Total cellular lipids rose ~25-fold, phosphatidylcholine increased from 23.5 to 57.9%, and PUFA:MUFA shifted; ferroptosis was proviral, and p10/FAST-driven syncytia increased LDs and showed ferroptosis hallmarks.

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