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Daral J. Jackwood - One of the best experts on this subject based on the ideXlab platform.
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molecular epidemiology of endemic and very virulent Infectious Bursal Disease virus genogroups in backyard chickens in california 2009 2017
Journal of Veterinary Diagnostic Investigation, 2019Co-Authors: Daral J. Jackwood, Simone A T Stoute, Beate M Crossley, L O MichelAbstract:Pathogenic strains of Infectious Bursal Disease virus (IBDV) are associated with increased morbidity, mortality, and immunosuppression in susceptible chickens. Backyard poultry is increasing in pop...
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a proposed nomenclature for Infectious Bursal Disease virus isolates
Avian Pathology, 2018Co-Authors: Daral J. Jackwood, Karel A Schat, L O Michel, Sjaak De WitAbstract:Infectious Bursal Disease virus (IBDV) was initially identified in the USA. For decades, these viruses were not categorized using a typing system because they were considered to be antigenically an...
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Classification of Infectious Bursal Disease virus into genogroups
Archives of Virology, 2017Co-Authors: L O Michel, Daral J. JackwoodAbstract:Infectious Bursal Disease virus (IBDV) causes Infectious Bursal Disease (IBD), an immunosuppressive Disease of poultry. The current classification scheme of IBDV is confusing because it is based on antigenic types (variant and classical) as well as pathotypes. Many of the amino acid changes differentiating these various classifications are found in a hypervariable region of the capsid protein VP2 (hvVP2), the major host protective antigen. Data from this study were used to propose a new classification scheme for IBDV based solely on genogroups identified from phylogenetic analysis of the hvVP2 of strains worldwide. Seven major genogroups were identified, some of which are geographically restricted and others that have global dispersion, such as genogroup 1. Genogroup 2 viruses are predominately distributed in North America, while genogroup 3 viruses are most often identified on other continents. Additionally, we have identified a population of genogroup 3 vvIBDV isolates that have an amino acid change from alanine to threonine at position 222 while maintaining other residues conserved in this genogroup (I242, I256 and I294). A222T is an important mutation because amino acid 222 is located in the first of four surface loops of hvVP2. A similar shift from proline to threonine at 222 is believed to play a role in the significant antigenic change of the genogroup 2 IBDV strains, suggesting that antigenic drift may be occurring in genogroup 3, possibly in response to antigenic pressure from vaccination.
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advances in vaccine research against economically important viral Diseases of food animals Infectious Bursal Disease virus
Veterinary Microbiology, 2017Co-Authors: Daral J. JackwoodAbstract:Numerous reviews have been published on Infectious Bursal Disease (IBD) and Infectious Bursal Disease virus (IBDV). Many high quality vaccines are commercially available for the control of IBD that, when used correctly, provide solid protection against infection and Disease caused by IBDV. Viruses are not static however; they continue to evolve and vaccines need to keep pace with them. The evolution of IBDV has resulted in very virulent strains and new antigenic types of the virus. This review will discuss some of the limitations associated with existing vaccines, potential solutions to these problems and advances in new vaccines for the control of IBD.
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viral competition and maternal immunity influence the clinical Disease caused by very virulent Infectious Bursal Disease virus
Avian Diseases, 2011Co-Authors: Daral J. JackwoodAbstract:SUMMARY. The very virulent form of Infectious Bursal Disease virus (vvIBDV) causes an immunosuppressive Disease that is further characterized by the rapid onset of morbidity and high mortality in susceptible chickens. In 2009, vvIBDV was first reported in California, U. S. A., and since that time only a few cases of acute Infectious Bursal Disease attributed to vvIBDV have been recognized in California. In other countries where vvIBDV has become established, it rapidly spreads to most poultry-producing regions. Two factors that may be involved in limiting the spread or reducing the severity of the clinical Disease caused by vvIBDV in the U. S. A. are maternal immunity and competition with endemic variant strains of the virus. In this study, the ability of vvIBDV to infect and cause Disease in maternally immune layer chickens was examined at weekly intervals over a 5-wk period during which their neutralizing maternal antibodies waned. Birds inoculated with vvIBDV at 2, 3, and 4 wk of age seemed healthy thr...
Egbert Mundt - One of the best experts on this subject based on the ideXlab platform.
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protective vaccination against Infectious Bursal Disease virus with whole recombinant kluyveromyces lactis yeast expressing the viral vp2 subunit
PLOS ONE, 2012Co-Authors: Marina Arnold, Egbert Mundt, Vijay Durairaj, Katja Schulze, Karin D Breunig, Svenerik BehrensAbstract:Here we report on vaccination approaches against Infectious Bursal Disease (IBD) of poultry that were performed with complete yeast of the species Kluyveromyces lactis (K. lactis). Employing a genetic system that enables the rapid production of stably transfected recombinant K. lactis, we generated yeast strains that expressed defined quantities of the virus capsid forming protein VP2 of Infectious Bursal Disease virus (IBDV). Both, subcutaneous as well as oral vaccination regiments with the heat-inactivated but otherwise untreated yeast induced IBDV-neutralizing antibodies in mice and chickens. A full protection against a subsequent IBDV infection was achieved by subcutaneous inoculation of only milligram amounts of yeast per chicken. Oral vaccination also generated protection: while mortality was observed in control animals after virus challenge, none of the vaccinees died and ca. one-tenth were protected as indicated by the absence of lesions in the bursa of Fabricius. Recombinant K. lactis was thus indicated as a potent tool for the induction of a protective immune response by different applications. Subcutaneously applied K. lactis that expresses the IBDV VP2 was shown to function as an efficacious anti-IBD subunit vaccine.
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current status of vaccines against Infectious Bursal Disease
Avian Pathology, 2012Co-Authors: Hermann J. Müller, Egbert Mundt, Nicolas Eterradossi, Rafiqul M IslamAbstract:Infectious Bursal Disease virus (IBDV) is the aetiological agent of the acute and highly contagious Infectious Bursal Disease (IBD) or "Gumboro Disease". IBD is one of the economically most important Diseases that affects commercially produced chickens worldwide. Along with strict hygiene management of poultry farms, vaccination programmes with inactivated and live attenuated viruses have been used to prevent IBD. Live vaccines show a different degree of attenuation; many of them may cause Bursal atrophy and thus immunosuppression with poor immune response to vaccination against other pathogens and an increase in vulnerability to various types of infections as possible consequences. Depending on their intrinsic characteristics or on the vaccination procedures, some of the vaccines may not induce full protection against the very virulent IBDV strains and antigenic variants observed in the last three decades. As chickens are most susceptible to IBDV in their first weeks of life, active immunity to the virus has to be induced early after hatching. However, maternally derived IBDV-specific antibodies may interfere with early vaccination with live vaccines. Thus new technologies and second-generation vaccines including rationally designed and subunit vaccines have been developed. Recently, live viral vector vaccines have been licensed in several countries and are reaching the market. Here, the current status of IBD vaccines is discussed.
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vp1 of Infectious Bursal Disease virus is an rna dependent rna polymerase
Journal of General Virology, 2004Co-Authors: Ursula I Von Einem, Svenerik Behrens, Alexander E Gorbalenya, Horst Schirrmeier, Tobias Letzel, Egbert MundtAbstract:Segment B of the bisegmented, double-stranded RNA genome of Infectious Bursal Disease virus (IBDV) encodes the viral protein VP1. This has been presumed to represent the RNA-dependent RNA polymerase (RdRp) as it contains motifs that are typical for the RdRp of plus-strand RNA viruses. Here it is demonstrated that baculovirus-expressed wild-type but not motif A mutated VP1 acts as an RdRp on IBDV-specific RNA templates. Thus, on a plus-strand IBDV segment A cRNA template, minus-strand synthesis occurred in such a way that a covalently linked double-stranded RNA product was generated (by a 'copy-back' mechanism). Importantly, enzyme activity was observed only with templates that comprised the 3' non-coding region of plus-strand RNAs transcribed from IBDV segments A and B, indicating template specificity. RdRp activity was shown to have a temperature optimum of 37 degrees C and required magnesium ions for enzyme activity. Thus, it has been demonstrated unequivocally that VP1 represents the RdRp of IBDV.
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Identification of a novel viral protein in Infectious Bursal Disease virus-infected cells.
Journal of General Virology, 1995Co-Authors: Egbert Mundt, Jörg Beyer, Hermann J. MüllerAbstract:Infectious Bursal Disease virus (IBDV), a member of the Birnaviridae, specifies two genomic double-stranded RNAs, segment A and segment B. Segment A encodes a 110 kDa polyprotein which is processed into virus proteins VP2, VP3 and VP4. A second open reading frame (ORF), designated ORF A-2, immediately preceding and partially overlapping the 110 kDa protein gene has also been described. After prokaryotic expression of this ORF and immunization of rabbits with the expressed protein we obtained reagents that allowed the identification of the ORF A-2 gene product in IBDV-infected cells. The ORF A-2 protein exhibits an apparent molecular mass of 21 kDa which is larger than the size of 16·5 kDa calculated from the deduced amino acid sequence. Immunofluorescence studies demonstrated the presence of the ORF A-2 protein in bursa samples from IBDV-infected chicken. In summary, the IBDV ORF A-2 product represents the fifth IBDV protein described. Therefore, we propose to designate it as IBDV VP5.
Jiangtao Zheng - One of the best experts on this subject based on the ideXlab platform.
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Reassortant Infectious Bursal Disease virus isolated in China.
Virus Research, 2007Co-Authors: Xuping Yu, Xiameng Yu, Jiangtao Zheng, Hong Xu, Lian YuAbstract:Abstract Infectious Bursal Disease virus (IBDV) is a bi-segmented, double-stranded RNA virus which belongs to the genus Avibirnavirus of the family Birnavirideae. In this study, we determined the complete nucleotide sequences of a reassortment IBDV strain TL2004 with segments A and B derived from attenuated and very virulent strains of IBDV. This strain is pathogenic to SPF-embryonated eggs and chickens, although it is not as virulent as very virulent strain. Genomic sequence in GenBank analysis showed that both types of natural genetic reassortment of Infectious Bursal Disease virus emerged in China. Our findings, which strongly suggest genetic exchange between attenuated and very virulent strains of IBDV, emphasizes the risk of generating uncontrolled chimeric viruses by using live attenuated vaccines.
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Genetic reassortment of Infectious Bursal Disease virus in nature.
Biochemical and biophysical research communications, 2006Co-Authors: Yongwei Wei, Jiangtao ZhengAbstract:Infectious Bursal Disease virus (IBDV), a double-stranded RNA virus, is a member of the Birnaviridae family. Four pathotypes of IBDV, attenuated, virulent, antigenic variant, and very virulent (vvIBDV), have been identified. We isolated and characterized the genomic reassortant IBDV strain ZJ2000 from severe field outbreaks in commercial flocks. Full-length genomic sequence analysis showed that ZJ2000 is a natural genetic reassortant virus with segments A and B derived from attenuated and very virulent strains of IBDV, respectively. ZJ2000 exhibited delayed replication kinetics as compared to attenuated strains. However, ZJ2000 was pathogenic to specific pathogen free (SPF) chickens and chicken embryos. Similar to a standard virulent IBDV strain, ZJ2000 caused 26.7% mortality, 100% morbidity, and severe Bursal lesions at both gross and histopathological levels. Taken together, our data provide direct evidence for genetic reassortment of IBDV in nature, which may play an important role in the evolution, virulence, and host range of IBDV. Our data also suggest that VP2 is not the sole determinant of IBDV virulence, and that the RNA-dependent RNA polymerase protein, VP1, may play an important role in IBDV virulence. The discovery of reassortant viruses in nature suggests an additional risk of using live IBDV vaccines, which could act as genetic donors for genome reassortment.
Susan E Sommerwagner - One of the best experts on this subject based on the ideXlab platform.
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amino acids contributing to antigenic drift in the Infectious Bursal Disease birnavirus ibdv
Virology, 2011Co-Authors: Daral J. Jackwood, Susan E SommerwagnerAbstract:We examined the effect of amino acids 222 and 254 on antigenicity of the variant Del-E strain of Infectious Bursal Disease virus (IBDV). Using molecular epidemiology, we identified a virus designated as Del-E-222 that was identical to Del-E except for alanine at position 222. A second virus was generated using reverse genetics of the Del-E backbone to create Del-E-254 that contained an asparagine at amino acid 254. The Del-E-222 and Del-E-254 viruses were tested for their ability to escape neutralizing immunity provided by parenteral vaccination. The bursas from birds vaccinated with parental Del-E and challenged with Del-E-222 or Del-E-254 had macroscopic lesions typical of an IBDV infection, and their B-BW ratios were significantly smaller than the controls. Microscopic lesions included lymphocyte depletion and confirmed the ability of Del-E-222 and Del-E-254 to break through the immunity induced by the parental Del-E virus vaccination. Both mutations appear to be contributing to antigenic drift.
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characteristics of a very virulent Infectious Bursal Disease virus from california
Avian Diseases, 2009Co-Authors: Daral J. Jackwood, Susan E Sommerwagner, Simone A T Stoute, Peter R Woolcock, Beate Crossley, Sharon K Hietala, B R CharltonAbstract:Abstract An outbreak of Infectious Bursal Disease (IBD) in two California layer flocks resulted in the isolation of two Infectious Bursal Disease viruses designated rA and rB. Increased mortality plus gross and histopathology in the layer flocks suggested rA and rB could be very virulent Infectious Bursal Disease virus (vvIBDV). Preliminary studies indicated that high mortality resulted when bursa homogenates from the layer farms were used to inoculate specific-pathogen-free (SPF) chicks. In addition, rA and rB contained VP2 amino acid sequences typically seen in vvIBDV. Molecular and in vivo studies were conducted to more thoroughly identify and characterize the rA and rB viruses. Nucleotide sequence analysis demonstrated that rA and rB had identical sequences across the hypervariable VP2 (hvVP2) and segment B regions examined, and their amino acid sequences in the hvVP2 region were identical to the vvIBDV type strains UK 661, OKYM, and Harbin. Furthermore, the genome segment B nucleotide sequences exami...
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the diagnosis of very virulent Infectious Bursal Disease in california pullets
Avian Diseases, 2009Co-Authors: Simone A T Stoute, Daral J. Jackwood, Susan E Sommerwagner, Peter R Woolcock, G L Cooper, Mark L Anderson, A A Bickford, Gabriel C Sentiescue, B R CharltonAbstract:Abstract This report documents the occurrence of a very virulent Infectious Bursal Disease virus (vvIBDV) in Northern California commercial brown pullets. Diagnosis was made from multiple accessions from two neighboring and epidemiologically related ranches submitted to the California Animal Health and Food Safety (CAHFS) laboratory. Pullets, 11 and 14 wk of age from ranch A (rA) and ranch B (rB) respectively, were submitted from Infectious Bursal Disease virus vaccinated flocks experiencing a drastic increase in mortality. The December 2008 outbreak resulted in 26% and 34% mortality on rA and rB respectively. Gross and histologic lesions characteristic of acute vvIBDV were observed. Gross lesions included edematous bursas, hemorrhages at the junction of the proventriculus and gizzard as well as hemorrhages on skeletal muscles. Microscopic lesions included severe lymphoid necrosis and inflammation in edematous bursas, lymphoid necrosis in thymus, spleen, Peyer's patches and cecal tonsils. Diagnosis of vvI...
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genetic characteristics of Infectious Bursal Disease viruses from four continents
Virology, 2007Co-Authors: Daral J. Jackwood, Susan E SommerwagnerAbstract:Following the initial discovery of very virulent Infectious Bursal Disease virus (vvIBDV) strains in Europe, these viruses spread to many parts of the world. In this study, we examined the phylogenetic relationship of never-before-published IBDV from 18 countries on four continents. All the samples were collected between 1997 and 2005 and were reported to be from broiler flocks experiencing higher than expected mortality which is often associated with acute very virulent Infectious Bursal Disease. A total of 113 samples were imported into the U.S. and viral genetic material was used to determine the nucleotide sequence of the VP2 gene hypervariable region. Although all the samples were reported to be associated clinically with high mortality, genetic analysis suggests that some were not vvIBDV strains. Two viruses from South Africa were genetically similar to U.S. variant viruses. A majority (71/113) of the viruses examined had the amino acid Alanine at position 222 and sixty-seven of these suspect vvIBDV also had amino acids I242, I256, I294 and S299 which are highly conserved among vvIBDV strains. Phylogenetic analysis placed putative vvIBDV strains from many different countries and geographic regions in a single clade with some minor non-significant branching.
Xuannian Wang - One of the best experts on this subject based on the ideXlab platform.
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Infectivity and propagation of attenuated Infectious Bursal Disease virus in the chicken B-lymphocyte cell line DT40
Archives of virology, 2009Co-Authors: Jun Luo, Gaiping Zhang, Jian-ming Fan, Man Teng, Leiming You, Ling Zhou, Ruiguang Deng, Xuannian Wang, Yanyan Yang, Li WangAbstract:In this paper, the infectivity and propagation of two attenuated Infectious Bursal Disease virus (IBDV) strains in DT40 cells were investigated. The results showed that both of the tested strains, TAD and HN3, directly infect and proliferate in DT40 cells, requiring no adaptive passages. Unexpectedly, IBDV can be rapidly propagated and continuously harvested at high titers for a long time, accompanied by the rapid growth of host cells and showing no increase in pathogenicity. Our results provide further support to suggest that DT40 cells can be used as an ideal model for studying IBDV pathogenesis. Additionally, the DT40 cell line could also serve as a potential system for commercial IBDV vaccine preparation.
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identification of neutralizing epitopes on the vp2 protein of Infectious Bursal Disease virus by phage displayed heptapeptide library screening and synthetic peptide mapping
Viral Immunology, 2005Co-Authors: Xuannian Wang, Gaiping Zhang, Yanyan Yang, Jiyong Zhou, Chunhua Feng, Junqing Guo, Hongxing Qiao, Dong Zhao, Guang Xu Xing, Ziliang WangAbstract:Infectious Bursal Disease virus (IBDV) is the causative agent of Infectious Bursal Disease, which is one of the most important and widespread Infectious Diseases in commercial chickens. Conformational epitopes have been reported in the highly variable region of the VP2 protein of IBDV. In the present study, a random heptapeptide library was screened by using monoclonal antibodies (mAbs), YNW17 and YNW29, directed to the VP2 of IBDV and two peptide motifs, D-X-P-R and A-R-G, were identified. The motifs are present on the N and C terminal sequences of the highly variable region of VP2. Synthetic overlapping peptides covering the motifs on VP2 were analyzed by Dot- ELISA with the mAbs and two epitopes 197CDSSDRPRVYTIT209 and 329ARGSLAVTI337 identified. The above epitopes were also recognized by chicken anti-IBDV sera and shown to inhibit the binding of their mAbs to recombinant VP2. Both mAbs and sera from mice immunized with the conjugated epitope-peptides were able to neutralize serotype I IBDV. These resu...
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identification of neutralizing epitopes on the vp2 protein of Infectious Bursal Disease virus by phage displayed heptapeptide library screening and synthetic peptide mapping
Viral Immunology, 2005Co-Authors: Xuannian Wang, Gaiping Zhang, Yanyan Yang, Jiyong Zhou, Chunhua Feng, Junqing Guo, Hongxing Qiao, Dong Zhao, Guang Xu Xing, Ziliang WangAbstract:Infectious Bursal Disease virus (IBDV) is the causative agent of Infectious Bursal Disease, which is one of the most important and widespread Infectious Diseases in commercial chickens. Conformational epitopes have been reported in the highly variable region of the VP2 protein of IBDV. In the present study, a random heptapeptide library was screened by using monoclonal antibodies (mAbs), YNW17 and YNW29, directed to the VP2 of IBDV and two peptide motifs, D-X-P-R and A-R-G, were identified. The motifs are present on the N and C terminal sequences of the highly variable region of VP2. Synthetic overlapping peptides covering the motifs on VP2 were analyzed by Dot- ELISA with the mAbs and two epitopes 197CDSSDRPRVYTIT209 and 329ARGSLAVTI337 identified. The above epitopes were also recognized by chicken anti-IBDV sera and shown to inhibit the binding of their mAbs to recombinant VP2. Both mAbs and sera from mice immunized with the conjugated epitope-peptides were able to neutralize serotype I IBDV. These results indicated that the epitopes are two neutralizing linear B-cell epitopes and would be useful for the development of peptide-based IBD vaccines.
