scholarly journals Induction of Apoptosis in Vitro by the 17-kDa Nonstructural Protein of Infectious Bursal Disease Virus: Possible Role in Viral Pathogenesis

Virology ◽  
2001 ◽  
Vol 285 (1) ◽  
pp. 50-58 ◽  
Author(s):  
Kun Yao ◽  
Vikram N. Vakharia
2001 ◽  
Vol 82 (5) ◽  
pp. 1107-1115 ◽  
Author(s):  
Annett Jungmann ◽  
Hermann Nieper ◽  
Hermann Müller

The kinetics of infectious bursal disease virus (IBDV) replication and induction of apoptosis were investigated in vitro and in vivo. After infection of chicken embryo (CE) cells with IBDV strain Cu-1, the proportion of apoptotic cells increased from 5·8% at 4 h post-infection (p.i.) to 64·5% at 48 h p.i. The proportion of apoptotic cells correlated with IBDV replication. UV-inactivated IBDV particles did not induce apoptosis. Double labelling revealed that, early after infection, the majority of antigen-expressing cells were not apoptotic; double-labelled cells appeared more frequently at later times. Remarkably, apoptotic cells were frequently located in the vicinity of antigen-expressing cells. This indicated that an apoptosis-inducing factor(s) might be released by cells that replicate IBDV. Since interferon (IFN) production has been demonstrated after IBDV infection, IFN was considered to be one of several factors. However, supernatants of infected CE cells in which virus infectivity had been neutralized were not sufficient to induce apoptosis.Similar results were observed in the infected bursae of Fabricius: early after infection, most of the cells either showed virus antigens or were apoptotic. Again, double-labelled cells appeared more frequently late after infection. This suggests that indirect mechanisms might also be involved in the induction of apoptosis in vivo, contributing to the rapid depletion of cells in the IBDV-infected bursa.


2006 ◽  
Vol 80 (7) ◽  
pp. 3369-3377 ◽  
Author(s):  
Meihong Liu ◽  
Vikram N. Vakharia

ABSTRACT Infectious bursal disease virus (IBDV), the causative agent of a highly contagious disease in chickens, carries a small nonstructural protein (NS). This protein has been implicated to play a role in the induction of apoptosis. In this study, we investigate the kinetics of viral replication during a single round of viral replication and examine the mechanism of IBDV-induced apoptosis. Our results show that it is caspase dependent and activates caspases 3 and 9. Nuclear factor kappa B (NF-κB) is also activated and is required for IBDV-induced apoptosis. The NF-κB inhibitor MG132 completely inhibited IBDV-induced DNA fragmentation, caspase 3 activation, and NF-κB activation. To study the function of the NS protein in this context, we generated the recombinant rGLS virus and an NS knockout mutant, rGLSNSΔ virus, using reverse genetics. Comparisons of the replication kinetics and markers for virally induced apoptosis indicated that the NS knockout mutant virus induces earlier and increased DNA fragmentation, caspase activity, and NF-κB activation. These results suggest that the NS protein has an antiapoptotic function at the early stage of virus infection.


2008 ◽  
Vol 70 (4) ◽  
pp. 407-410 ◽  
Author(s):  
Kaori TERASAKI ◽  
Haruko HIRAYAMA ◽  
Christopher J. KASANGA ◽  
Min Thein MAW ◽  
Kenji OHYA ◽  
...  

2004 ◽  
Vol 105 (1) ◽  
pp. 23-34 ◽  
Author(s):  
Kati Zierenberg ◽  
Rüdiger Raue ◽  
Hermann Nieper ◽  
Md.Rafiqul Islam ◽  
Nicolas Eterradossi ◽  
...  

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