Abstract
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 μ m ) 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.