Effective multiple oral administration of reverse genetics engineered infectious bursal disease virus in mice in the presence of neutralizing antibodies

2015 ◽  
Vol 17 (6-7) ◽  
pp. 116-131 ◽  
Author(s):  
Ákos Hornyák ◽  
Kai S. Lipinski ◽  
Tamás Bakonyi ◽  
Petra Forgách ◽  
Ernő Horváth ◽  
...  
Keyword(s):  
Oral Administration ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Neutralizing Antibodies ◽  
Reverse Genetics ◽  
Infectious Bursal Disease ◽  
Bursal Disease

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.

scholarly journals The expression in plants of an engineered VP2 protein of Infectious Bursal Disease Virus induces formation of structurally heterogeneous particles that protect from a very virulent viral strain

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247134
Author(s):  
Carla Marusic ◽  
Charifa Drissi Touzani ◽  
Alessio Bortolami ◽  
Marcello Donini ◽  
Claudia Zanardello ◽  
...  
Keyword(s):  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Neutralizing Antibodies ◽  
Sucrose Density Gradient ◽  
Bursa Of Fabricius ◽  
Infectious Bursal Disease ◽  
Structural Protein ◽  
Vp2 Protein ◽  
Bursal Disease ◽  
Specific Pathogen

Infectious Bursal Disease Virus (IBDV), the etiological agent of Gumboro disease, causes mortality and immunosuppression in chickens and major losses to poultry industry worldwide. The IBDV major capsid protein VP2 is considered the best candidate for the production of novel subunit vaccines. This structural protein contains the major conformational epitopes responsible for the induction of IBDV neutralizing antibodies in chickens and has been demonstrated able to form supramolecular structures in yeast and insect cells. The aim of this study was to express an engineered version of the VP2 protein (His-pVP2) to verify its ability to self-assemble into virus-like particles in plants. The recombinant VP2 was transiently expressed by agroinfiltration in Nicotiana benthamiana and transmission electron microscopy of sucrose density gradient fractions revealed the presence of a mixed population of differently shaped particles ranging from spherical capsids, with a diameter between ~25 and ~70 nm, to tubular structures, with variable length (from 100 to 400 nm). The recombinant VP2-based particles when used for the intramuscular immunization of specific-pathogen-free chicks resulted able to induce the production of anti-IBDV specific antibodies at titers comparable to those induced by a commercial vaccine. Moreover, all the immunized birds survived to the challenge with a Moroccan very virulent IBDV strain with no major histomorphological alterations of the Bursa of Fabricius, similarly to what obtained with the commercial inactivated vaccine.

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.

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