Cytokine-like-Vago-mediated antiviral response in Penaeus monodon via IKK-NF-κB signaling pathway

Abstract

Interferon (IFN) system is the primary mechanism of innate antiviral defense in immune response. To date, limited studies of IFN system were conducted in crustaceans. Previous report in Penaeus monodon demonstrated the interconnection of cytokine-like molecule Vago and inhibitor of kappa B kinase-nuclear factor κB (IKK-NF-κB) cascade against white spot syndrome virus (WSSV). This study further identified five different PmVago isoforms. Upon immune stimulation, PmVagos expressed against shrimp pathogens. PmVago1, PmVago4 , and PmVago5 highly responded to WSSV, whereas, PmVago1 and PmVago4 RNAi exhibited a rapid mortality with elevated WSSV replication. Suppression of PmVago1 and PmVago4 negatively affected proPO system, genes in signal transduction, and AMPs. WSSV infection additionally induced Pm Vaog4 granule accumulation and cellular translocation to the area of cell membrane. More importantly, PmVago1 and PmVago4 promoters were stimulated by Pm IKK overexpression; meanwhile, they further activated Dorsal and Relish promoter activities. These results suggested the possible roles of the cytokine-like PmVago via IKK-NF-κB cascade against WSSV infection. • WSSV induced Vago accumulation in area of hemocyte membrane and granules • Vago1 and Vago4 RNAi increased shrimp cumulative mortality and WSSV replication • Vago associated with gene transcription in Toll, IMD, JAK/STAT pathways, and PO system • Vago1 and Vago4 stimulated NF-κB homologs Dorsal and Relish via IKK-NF-κB cascade Immunology; Virology

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