Chimeras in noncoding regions between serotypes I and II of segment A of infectious bursal disease virus are viable and show pathogenic phenotype in chickens

Microbiology ◽  
2000 ◽  
Vol 81 (2) ◽  
pp. 533-540 ◽  
Author(s):  
Anja Schröder ◽  
Adriaan A. W. M. van Loon ◽  
Danny Goovaerts ◽  
Egbert Mundt
Keyword(s):  
Cell Culture ◽  
Disease Virus ◽  
Cdna Clone ◽  
Infectious Bursal Disease Virus ◽  
Reverse Genetics ◽  
Infectious Bursal Disease ◽  
Noncoding Regions ◽  
The Family ◽  
Bursal Disease ◽  
Chimeric Viruses

Two serotypes, I and II, have been identified for infectious bursal disease virus (IBDV), a member of the family Birnaviridae. Here, the generation by reverse genetics of IBDV chimeras in segment A of the bisegmented genome is reported. The 5- and 3′-noncoding regions (NCRs) of a serotype II strain were exchanged with the NCRs of a full-length cDNA clone of segment A of a serotype I strain. Isolated chimeric viruses were characterized in cell culture and susceptible chickens. The results show that IBDV chimeras in segment A were able to replicate in cell culture and that VP1 encoded by a serotype I segment B is functionally active with serotype I NCRs as well as with serotype II NCRs. Chimeric viruses infected susceptible chickens and caused mild depletion of bursal cells. Thus, the noncoding regions of segment A are not responsible for the different pathotypes of IBDV serotypes I and II.

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 Molecular and Structural Bases for the Antigenicity of VP2 of Infectious Bursal Disease Virus

2007 ◽  
Vol 81 (23) ◽  
pp. 12827-12835 ◽  
Author(s):  
Tobias Letzel ◽  
Fasseli Coulibaly ◽  
Felix A. Rey ◽  
Bernard Delmas ◽  
Erik Jagt ◽  
...  
Keyword(s):  
Amino Acids ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Reverse Genetics ◽  
The United States ◽  
Antigenic Drift ◽  
Infectious Bursal Disease ◽  
Antigenic Determinants ◽  
Vp2 Gene ◽  
Bursal Disease

ABSTRACT Infectious bursal disease virus (IBDV), a member of the family Birnaviridae, is responsible for a highly contagious and economically important disease causing immunosuppression in chickens. IBDV variants isolated in the United States exhibit antigenic drift affecting neutralizing epitopes in the capsid protein VP2. To understand antigenic determinants of the virus, we have used a reverse-genetics approach to introduce selected amino acid changes—individually or in combination—into the VP2 gene of the classical IBDV strain D78. We thus generated a total of 42 mutants with changes in 8 amino acids selected by sequence comparison and their locations on loops PBC and PHI at the tip of the VP2 spikes, as shown by the crystal structure of the virion. The antibody reactivities of the mutants generated were assessed using a panel of five monoclonal antibodies (MAbs). Our results show that a few amino acids of the projecting domain of VP2 control the reactivity pattern. Indeed, the binding of four out of the five MAbs analyzed here is affected by mutations in these loops. Furthermore, their importance is highlighted by the fact that some of the engineered mutants display identical reactivity patterns but have different growth phenotypes. Finally, this analysis shows that a new field strain isolated from a chicken flock in Belgium (Bel-IBDV) represents an IBDV variant with a hitherto unobserved antigenic profile, involving one change (P222S) in the PBC loop. Overall, our data provide important new insights for devising efficient vaccines that protect against circulating IBDV strains.

Inhibition of Infectious Bursal Disease Virus by Vector Delivered SiRNA in Cell Culture

2014 ◽  
Vol 26 (1) ◽  
pp. 58-64 ◽  
Author(s):  
Amol Ashok Sahare ◽  
Megha Kadam Bedekar ◽  
Sudhir Kumar Jain ◽  
Azad Singh ◽  
Sanjeev Singh ◽  
...  
Keyword(s):  
Cell Culture ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Bursal Disease
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