Aquatic birnavirus induces necrotic cell death via the mitochondria-mediated caspase pathway

Po Chun Chen, Jen Leih Wu, Guor Mour Her, Jiann Ruey Hong

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)


Aquatic birnavirus induces necrotic cell death by an ill-understood process. Presently, we demonstrate that infectious pancreatic necrosis virus (IPNV) induces post-apoptotic necrotic cell death through loss of mitochondrial membrane potential (MMP) followed by caspase-3 activation in CHSE-214 cells. Progressive phosphatidylserine externalization was observed at 6 h post-infection (p.i.). This was followed by the development of bulb-like vesicles (bleb formation) at 8 h p.i. Progressive loss of MMP was also observed in IPNV-infected CHSE-214 cells beginning at 6 h p.i. At 8 h and 12 h p.i., IPNV-infected cells demonstrated a dramatic increase in MMP loss, rapid entry into necrotic cell death, and activation of caspase-9 and -3. Additionally, treatment with an inhibitor of MMP loss, bongkrekic acid, an adenine nucleotide translocase inhibitor, blocked IPNV-induced PS exposure and MMP loss, as well as reduced the activation of caspase-3. Taken together, our results suggest that IPNV induces apoptotic cell death via loss of MMP, thereby triggering secondary necrosis and caspases-3 activation. Furthermore, this death-signaling pathway is disrupted by bongkrekic acid in fish cells, indicating that this drug may serve to modulate IPNV-induced pathogenesis.

Original languageEnglish
Pages (from-to)344-353
Number of pages10
JournalFish and Shellfish Immunology
Issue number2
Publication statusPublished - 2010 Feb

All Science Journal Classification (ASJC) codes

  • Environmental Chemistry
  • Aquatic Science


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