Singapore grouper iridovirus VP018 exploits FTR86 to promote viral replication through Tollip-mediated degradation of the STING-TBK1 axis.

EcFTR86, a fish-specific TRIM protein in Epinephelus coioides, is up-regulated by SGIV and promotes viral replication by degrading STING or TBK1.

• Why it matters: Fish-specific FTR proteins lack mammalian counterparts, leaving how they shape innate antiviral signaling during iridovirus infection unclear.
• What they did: The study mapped EcFTR86 to lysosomes, tested SGIV replication after EcFTR86 overexpression or knockdown, and used interaction and degradation assays to show autophagy-lysosome–dependent turnover of STING/TBK1 via Tollip.
• The result: VP018, but not VP075, exploits EcFTR86 to accelerate STING/TBK1 degradation and abrogate type I interferon signaling, enabling SGIV replication in grouper spleen cells.

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