Ftz-F1H promotes white spot syndrome virus infection in shrimp by suppressing the Dorsal pathway

White spot syndrome virus (WSSV) is currently a major viral pathogen of cultured shrimp. The NF-KB signaling is central to the regulation of immune responses in both invertebrates and vertebrates. Dorsal is a member of the NF-KB family in arthropods, playing important role in shrimp antiviral response. The fushi tarazu (FTZ) transcription factor (Ftz-F1) homologue (Ftz-F1H) is a novel identified orphan nuclear receptor in Pacific white shrimp Penaeus vannamei with an inhibitory effect on anti-Vibrio parahaemolyticus response. The current study investigated the role of Ftz-F1H in the immune response against WSSV infection. We showed that Ftz-F1H directly promoted the expression of Cactus, the cytoplasmic inhibitor of the Dorsal pathway in shrimp, and inhibited the nuclear translocation of Dorsal. Silencing of Ftz-F1H in vivo suppressed the WSSV infection in shrimp. These suggested that Ftz-F1H could promote WSSV infection by inhibiting the activation of the Dorsal pathway. This study, together with the previous finding, indicated that inhibition of Ftz-F1H in shrimp could enhance the defense against both bacterial and viral infections.

Automated summary

The NF-KB signaling pathway plays a crucial role in the immune response of shrimp, while Ftz-F1H is involved in antiviral response, promoting WSSV infection by inhibiting the activation of the Dorsal pathway.