Further evidence for the association of distinct amino acid residues with in vitro and in vivo growth of infectious bursal disease virus

2013 ◽  
Vol 159 (4) ◽  
pp. 701-709 ◽  
Author(s):  
M. Noor ◽  
M. S. Mahmud ◽  
P. R. Ghose ◽  
U. Roy ◽  
M. Nooruzzaman ◽  
...  
Keyword(s):  
Amino Acid ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Amino Acid Residues ◽  
Bursal Disease ◽  
In Vivo Growth

Generation of serotype 1/serotype 2 reassortant viruses of the infectious bursal disease virus and their investigation in vitro and in vivo

2004 ◽  
Vol 105 (1) ◽  
pp. 23-34 ◽  
Author(s):  
Kati Zierenberg ◽  
Rüdiger Raue ◽  
Hermann Nieper ◽  
Md.Rafiqul Islam ◽  
Nicolas Eterradossi ◽  
...  
Keyword(s):  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Bursal Disease ◽  
Serotype 1 ◽  
Reassortant Viruses

scholarly journals Apoptosis is induced by infectious bursal disease virus replication in productively infected cells as well as in antigen-negative cells in their vicinity

2001 ◽  
Vol 82 (5) ◽  
pp. 1107-1115 ◽  
Author(s):  
Annett Jungmann ◽  
Hermann Nieper ◽  
Hermann Müller
Keyword(s):  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Virus Infectivity ◽  
Double Labelling ◽  
Apoptotic Cells ◽  
Bursal Disease ◽  
Induction Of Apoptosis

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.

scholarly journals VP5 and the N terminus of VP2 are not responsible for the different pathotype of serotype I and II infectious bursal disease virus

2001 ◽  
Vol 82 (1) ◽  
pp. 159-169 ◽  
Author(s):  
Anja Schröder ◽  
Adriaan A. W. M. van Loon ◽  
Danny Goovaerts ◽  
Jens Peter Teifke ◽  
Egbert Mundt
Keyword(s):  
B Lymphocytes ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Reverse Genetics ◽  
Bursa Of Fabricius ◽  
Infectious Bursal Disease ◽  
Bursal Disease ◽  
Chimeric Viruses

Two serotypes have been identified in infectious bursal disease virus (IBDV), a member of the family Birnaviridae. A reverse genetics system was used for generation of chimeras in genome segment A of the two serotypes, in which the complete viral VP5 gene and 3′ noncoding region (NCR), or parts thereof, were exchanged. The engineered viruses were characterized in vitro and in vivo in comparison to serotype I and II IBDV. Our results show that IBDV chimeras exhibit a different phenotype in cell culture compared to the wild-type viruses. In in vitro-cultivated bursal-derived cells, chimeric viruses infected B lymphocytes, as does serotype I IBDV. Surprisingly, serotype II virus was also able to infect in vitro-cultivated bursal cells, but these were neither B lymphocytes nor macrophages. After infection of susceptible chickens all chimeras replicated in the bursa of Fabricius (BF), and three chimeric viruses caused mild depletion of bursal cells. In contrast, after infection of chickens with a chimeric IBDV containing exchanged VP5 as well as 3′-NCR, no depletion was detectable. The serotype II strain did not replicate in the BF nor did it cause depletion of bursal cells. Thus, the origin of VP5 does not explain the different pathotype of IBDV serotype I and II.

scholarly journals Generation of a Mutant Infectious Bursal Disease Virus That Does Not Cause Bursal Lesions

1998 ◽  
Vol 72 (4) ◽  
pp. 2647-2654 ◽  
Author(s):  
Kun Yao ◽  
Mark A. Goodwin ◽  
Vikram N. Vakharia
Keyword(s):  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Clinical Signs ◽  
Mutant Virus ◽  
Infectious Bursal Disease ◽  
Nucleotide Sequence Analysis ◽  
Fluorescence Signal ◽  
Bursal Disease

ABSTRACT A reverse genetics system for birnavirus, based on synthetic transcripts of the infectious bursal disease virus (IBDV) genome, was recently developed (E. Mundt and V. N. Vakharia, Proc. Natl. Acad. Sci. USA 93:11131–11136, 1996). To study the function of the 17-kDa nonstructural (NS) protein in viral growth and pathogenesis, we constructed a cDNA clone of IBDV segment A in which the first and only initiation codon (ATG) of NS protein was mutated to a stop codon (TAG). Transfection of Vero cells with combined transcripts of either modified or unmodified segment A, and with segment B, generated viable IBDV progeny. When chicken embryo fibroblast cells infected with transfectant viruses were analyzed by immunofluorescence assays using NS-specific antiserum, the mutant virus did not yield a fluorescence signal, indicating a lack of NS protein expression. Furthermore, replication kinetics and cytotoxic effects of the mutant virus were compared with those of the parental attenuated vaccine strain of IBDV (D78) in vitro. The mutant virus grew to slightly lower titers than D78 virus and exhibited decreased cytotoxic and apoptotic effects in cell culture. To evaluate the characteristics of the recovered viruses in vivo, we inoculated 3-week-old chickens with D78 or mutant virus and analyzed their bursa for histopathological lesions. The recovered D78 virus caused microscopic lesions and atrophy of the bursa, while the mutant virus failed to induce any pathological lesions or clinical signs of disease. In both instances, the virus was recovered from the bursa, and the presence or absence of mutation in these viruses was confirmed by nucleotide sequence analysis of NS gene. Although the mutant virus exhibited a delay in replication in vivo, it induced levels of IBDV neutralizing antibodies that were similar to those of D78 virus. In addition, no reversion of mutation was detected in the mutant virus recovered from inoculated chickens. These results demonstrate that NS protein is dispensable for viral replication in vitro and in vivo and that it plays an important role in viral pathogenesis. Thus, generation of such NS protein-deficient virus will facilitate the study of immunosuppression and aid in the development of live-attenuated vaccines for IBDV.

scholarly journals TRIM25 inhibits infectious bursal disease virus replication by targeting VP3 for ubiquitination and degradation

2021 ◽  
Vol 17 (9) ◽  
pp. e1009900
Author(s):  
Suyan Wang ◽  
Mengmeng Yu ◽  
Aijing Liu ◽  
Yuanling Bao ◽  
Xiaole Qi ◽  
...  
Keyword(s):  
Viral Replication ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Defense Responses ◽  
Immune Defense ◽  
Infectious Bursal Disease ◽  
Structural Protein ◽  
Bursal Disease

Infectious bursal disease virus (IBDV), a double-stranded RNA virus, causes immunosuppression and high mortality in 3–6-week-old chickens. Innate immune defense is a physical barrier to restrict viral replication. After viral infection, the host shows crucial defense responses, such as stimulation of antiviral effectors to restrict viral replication. Here, we conducted RNA-seq in avian cells infected by IBDV and identified TRIM25 as a host restriction factor. Specifically, TRIM25 deficiency dramatically increased viral yields, whereas overexpression of TRIM25 significantly inhibited IBDV replication. Immunoprecipitation assays indicated that TRIM25 only interacted with VP3 among all viral proteins, mediating its K27-linked polyubiquitination and subsequent proteasomal degradation. Moreover, the Lys854 residue of VP3 was identified as the key target site for the ubiquitination catalyzed by TRIM25. The ubiquitination site destroyed enhanced the replication ability of IBDV in vitro and in vivo. These findings demonstrated that TRIM25 inhibited IBDV replication by specifically ubiquitinating and degrading the structural protein VP3.

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