Abstract:
:In this study, we show how the red spotted grouper nervous necrosis virus (RGNNV) causes loss of mitochondrial membrane potential and promotes host secondary apoptotic necrosis. RGNNV viral proteins such as protein alpha (42 kDa) and protein A (110 kDa) were quickly expressed between 12 h and 24 h postinfection (p.i.) in GL-av cells. Annexin V staining revealed that the NNV infection of GL-av cells induced phosphatidylserine (PS) externalization and development of bulb-like vesicles (bleb formation) at 24 h p.i. NNV infection also induced DNA fragmentation detectable by TUNEL assay between 12 h (8%) and 72 h (32%) p.i. Bongkrekic acid (1.6 microM; BKA) blocked permeability of the mitochondrial permeability transition pore, but cyclosporine A (CsA) did not block secondary necrosis. Finally, secondary necrotic cells were not engulfed by neighboring cells. Our data suggest that RGNNV induces apoptotic death via opening the mitochondrial permeability transition pore thereby triggering secondary necrosis in the mid-apoptotic phase.
journal_name
Virologyjournal_title
Virologyauthors
Chen SP,Yang HL,Her GM,Lin HY,Jeng MF,Wu JL,Hong JRdoi
10.1016/j.virol.2005.11.052subject
Has Abstractpub_date
2006-04-10 00:00:00pages
379-91issue
2eissn
0042-6822issn
1096-0341pii
S0042-6822(05)00797-Xjournal_volume
347pub_type
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