scholarly journals Tissue culture infectivity of different strains of infectious bursal disease virus is determined by distinct amino acids in VP2

1999 ◽  
Vol 80 (8) ◽  
pp. 2067-2076 ◽  
Author(s):  
Egbert Mundt
Keyword(s):  
Amino Acids ◽  
Tissue Culture ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Reverse Genetics ◽  
Site Directed Mutagenesis ◽  
Bursa Of Fabricius ◽  
Infectious Bursal Disease ◽  
Embryonic Cells ◽  
Bursal Disease

Two types of strains of serotype I of infectious bursal disease virus (IBDV) have been described, on the basis of their ability (IBDV-TC) or inability (IBDV-BU) to infect chicken embryonic cells in culture. However, both types infect B lymphocytes in the bursa of Fabricius of young chickens. To determine the molecular basis for tissue culture infectivity, virus recombinants with chimeric segments A were constructed from IBDV-TC and IBDV-BU by reverse genetics. The region responsible for the different phenotypes was located in VP2. Site-directed mutagenesis identified single amino acids that are responsible for the restriction in infectivity. However, the appropriate amino acid exchanges are strain-specific.

scholarly journals Alteration of amino acids in VP2 of very virulent infectious bursal disease virus results in tissue culture adaptation and attenuation in chickens

2002 ◽  
Vol 83 (1) ◽  
pp. 121-129 ◽  
Author(s):  
A. A. W. M. van Loon ◽  
N. de Haas ◽  
I. Zeyda ◽  
E. Mundt
Keyword(s):  
Amino Acids ◽  
Tissue Culture ◽  
Amino Acid ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Site Directed Mutagenesis ◽  
Infectious Bursal Disease ◽  
Single Amino Acid ◽  
Culture Adaptation ◽  
Bursal Disease

Reverse genetics technology offers the possibility to study the influence of particular amino acids of infectious bursal disease virus (IBDV) on adaptation to tissue culture. Genomic segments A and B of the very virulent (vv) IBDV field strain UK661 were completely cloned and sequenced, and the strain was rescued from full-length cDNA copies of both segments (UK661rev). Using site-directed mutagenesis, alteration of a single amino acid in the segment A-encoded VP2 (A284T) resulted in a limited capacity of UK661 to replicate in tissue culture. Additional alteration of a second amino acid (Q253H) increased replication efficiency in tissue culture. The second mutant (UK661-Q253H-A284T) was used to infect chickens and results were compared with UK661 and UK661rev. Whereas UK661 and UK661rev induced 100% morbidity and 50–80% mortality, UK661-Q253H-A284T proved to be strikingly attenuated, producing neither morbidity nor mortality. Moreover, UK661-Q253H-A284T-infected animals were protected from challenge infection. Thus, alteration of two specific amino acids in the VP2 region of IBDV resulted in tissue culture adaptation and attenuation in chickens of vvIBDV. The data demonstrate that VP2 plays a decisive role in pathogenicity of IBDV.

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 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 Genome-wide analysis of differentially expressed mRNAs, lncRNAs, and circRNAs in chicken bursae of Fabricius during infection with very virulent infectious bursal disease virus

BMC Genomics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Xuewei Huang ◽  
Junyan Zhang ◽  
Zengsu Liu ◽  
Meng Wang ◽  
Xiaolong Fan ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Expression Profiles ◽  
Circular Rna ◽  
Differentially Expressed ◽  
Bursa Of Fabricius ◽  
Infectious Bursal Disease ◽  
Non Coding Rna ◽  
Bursal Disease

Abstract Background Infectious bursal disease virus (IBDV) causes acute, highly contagious, immunosuppressive, and lethal infectious disease in young chickens and mainly infects the bursa of Fabricius (BF). To investigate interactions between IBDV and its host, RNA sequencing was applied to analyze the responses of the differentially expressed transcriptional profiles of BF infected by very virulent IBDV (vvIBDV). Results In total, 317 upregulated and 94 downregulated mRNAs were found to be significantly differentially expressed in infected chickens, compared to controls. Long non-coding RNA (lncRNA) and circular RNA (circRNA) alterations were identified in IBDV-infected chickens, and significantly different expression was observed in 272 lncRNAs and 143 circRNAs. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed to assess the functions of significantly dysregulated genes, which showed that the JAK-STAT signaling pathway, the NOD-like receptor signaling pathway, and apoptosis may be activated by IBDV infection. We predicted interactions between differentially expressed genes and produced lncRNA-mRNA and circRNA-miRNA-mRNA regulator network. Conclusions The present study identified the expression profiles of mRNAs, lncRNAs, and circRNAs during vvIBDV infection and provides new insights into the pathogenesis of IBDV and antiviral immunity of the host.

Sign in / Sign up

Export Citation Format

Share Document