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

• Published in: Journal of fish diseases 2008-06, Vol.31 (6), p.451-460
• Main Authors: Hong, J-R, Guan, B-J, Her, G M, Evensen, O, Santi, N, Wu, J-L
• Format: Article
• Language: English
• Subjects: Birnavirus; Infectious pancreatic necrosis virus
• ISSN: 0140-7775; 1365-2761
• DOI: 10.1111/j.1365-2761.2008.00928.x

AbstractOur 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-B 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-B is apparently activated 6-8h post-IPNV infection. Using genistein (100kgmL-1; a tyrosine kinase inhibitor) to determine whether NF-B activation requires tyrosine kinase activation, we found genistein blocks NF-B activation at 8h post-infection (p.i), and either enhances cell viability up to 50% at 12h p.i. or blocks DNA fragmentation at 24h p.i. Furthermore, the proteasome inhibitors PSI-I and PSI-II (both at 40km) also effectively blocked the NF-B activation as well as stimulating a 30% increase in cell viability (30% decrease in apoptosis) at 8 and 12h p.i. Taken together our data suggest that IPNV may induce NF-B activation through tyrosine kinase signalling, which may be associated with induction of apoptosis.