Yellow fever virus infection triggers the assembly of compositionally unique and specialised stress granules.

Yellow fever virus infection (17D vaccine and Asibi strains) induces translational shut-off and stress granules at 48 hpi, despite viral detection by 24 hpi.

• Why it matters: Stress granules link cellular stress control to innate immune activation, but their specific role during yellow fever virus infection was unclear.
• What they did: The study inhibited stress granule assembly with a small-molecule inhibitor and siRNA knockdown, then profiled the stress granule proteome and assessed mitochondrial damage and dysfunction.
• The result: Stress granule formation did not affect viral replication, but silencing G3BP1 and other scaffolds increased ISG expression; virus-induced stress granules had a unique composition enriched for mitochondrial proteins.

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