Tissue distribution and developmental changes of interferon regulatory factors in chickens and effects of infectious bursal disease virus infection

2020 ◽  
pp. 104601
Author(s):  
Yan Yu ◽  
Lingling Cheng ◽  
Zhiyong Xu ◽  
Yanhong Zhang ◽  
Changbo Ou ◽  
...  
Keyword(s):  
Virus Infection ◽  
Tissue Distribution ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Developmental Changes ◽  
Infectious Bursal Disease ◽  
Regulatory Factors ◽  
Interferon Regulatory Factors ◽  
Bursal Disease

scholarly journals Western blot detection of infectious bursal disease virus infection

1998 ◽  
Vol 31 (5) ◽  
pp. 671-674 ◽  
Author(s):  
S.R.F.G. Pereira ◽  
C.E.P.F. Travassos ◽  
A. Huguenim ◽  
A.C.C. Guimarães ◽  
A.G. Silva ◽  
...  
Keyword(s):  
Virus Infection ◽  
Western Blot ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Bursal Disease

scholarly journals Nonstructural Protein of Infectious Bursal Disease Virus Inhibits Apoptosis at the Early Stage of Virus Infection

2006 ◽  
Vol 80 (7) ◽  
pp. 3369-3377 ◽  
Author(s):  
Meihong Liu ◽  
Vikram N. Vakharia
Keyword(s):  
Virus Infection ◽  
Dna Fragmentation ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Early Stage ◽  
Nonstructural Protein ◽  
Infectious Bursal Disease ◽  
Knockout Mutant ◽  
Bursal Disease ◽  
Induced Apoptosis

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.

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