Aquatic birnavirus infection activates the transcription factor NF-κB via tyrosine kinase signalling leading to cell death

Our previous studies found that infectious pancreatic necrosis virus (IPNV) induces host apoptotic cell death, possibly through a newly synthesized protein trigger. Here, we examine whether IPNV infection can induce NF-κB activation through tyrosine kinase signalling of CHSE-214 cell death (host cell death). Using the electrophoretic mobility shift assay (EMSA) to detect transcription factor activation, we found that NF-κB is apparently activated 6-8 h post-IPNV infection. Using genistein (100 μg mL^-1; a tyrosine kinase inhibitor) to determine whether NF-κB activation requires tyrosine kinase activation, we found genistein blocks NF-κB activation at 8 h post-infection (p.i), and either enhances cell viability up to 50% at 12 h p.i. or blocks DNA fragmentation at 24 h p.i. Furthermore, the proteasome inhibitors PSI-I and PSI-II (both at 40 μm) also effectively blocked the NF-κB activation as well as stimulating a 30% increase in cell viability (30% decrease in apoptosis) at 8 and 12 h p.i. Taken together our data suggest that IPNV may induce NF-κB activation through tyrosine kinase signalling, which may be associated with induction of apoptosis.