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

Schröder, AC; Loon, A.A. van; Goovaerts, D.; Mundt, Egbert

doi:10.1099/0022-1317-81-2-533

Cited by 29 publications

(26 citation statements)

References 28 publications

(56 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the mirror experiment remains to be performed and it cannot be excluded that introducing partial or full length NCRs of Cu-1 in the B88 segment would also result in attenuation. Altogether, these results can hardly compare with a previous study by Schröder et al [69], [70], showing that incorporating segment A NCRs derived from an apathogenic serotype 2 IBDV strain into the genetic context of a cell culture adapted serotype 1 virus reduced the in vitro replication ability but only had a limited influence on bursal lesions. The different impact of the NCR exchange is most probably due to the secondary structures of the exchanged NCRs being very different in the two studies (inter-serotypic exchange in Schröder et al, intra-serotypic exchange in the present work).…”

Section: Discussioncontrasting

confidence: 77%

Different Domains of the RNA Polymerase of Infectious Bursal Disease Virus Contribute to Virulence

et al. 2012

View full text Add to dashboard Cite

BackgroundInfectious bursal disease virus (IBDV) is a pathogen of worldwide significance to the poultry industry. IBDV has a bi-segmented double-stranded RNA genome. Segments A and B encode the capsid, ribonucleoprotein and non-structural proteins, or the virus polymerase (RdRp), respectively. Since the late eighties, very virulent (vv) IBDV strains have emerged in Europe inducing up to 60% mortality. Although some progress has been made in understanding the molecular biology of IBDV, the molecular basis for the pathogenicity of vvIBDV is still not fully understood.Methodology, Principal FindingsStrain 88180 belongs to a lineage of pathogenic IBDV phylogenetically related to vvIBDV. By reverse genetics, we rescued a molecular clone (mc88180), as pathogenic as its parent strain. To study the molecular basis for 88180 pathogenicity, we constructed and characterized in vivo reassortant or mosaic recombinant viruses derived from the 88180 and the attenuated Cu-1 IBDV strains. The reassortant virus rescued from segments A of 88180 (A88) and B of Cu-1 (BCU1) was milder than mc88180 showing that segment B is involved in 88180 pathogenicity. Next, the exchange of different regions of BCU1 with their counterparts in B88 in association with A88 did not fully restore a virulence equivalent to mc88180. This demonstrated that several regions if not the whole B88 are essential for the in vivo pathogenicity of 88180.Conclusion, SignificanceThe present results show that different domains of the RdRp, are essential for the in vivo pathogenicity of IBDV, independently of the replication efficiency of the mosaic viruses.

show abstract

Section: Discussioncontrasting

confidence: 77%

Different Domains of the RNA Polymerase of Infectious Bursal Disease Virus Contribute to Virulence

et al. 2012

View full text Add to dashboard Cite

show abstract

“…The severity of bursal follicular necrosis was recorded using the average histopathological bursa lesion score (HBLS) system as described previously [34].…”

Section: Methodsmentioning

confidence: 99%

Mutations of Residues 249 and 256 in VP2 Are Involved in the Replication and Virulence of Infectious Bursal Disease Virus

Zhang

Chen

et al. 2013

PLoS ONE

View full text Add to dashboard Cite

Infectious bursal disease virus (IBDV) is a pathogen of worldwide significance to the poultry industry. Although the PDE and PFG domains of the capsid protein VP2 contribute significantly to virulence and fitness, the detailed molecular basis for the pathogenicity of IBDV is still not fully understood. Because residues 253 and 284 of VP2 are not the sole determinants of virulence, we hypothesized that other residues involved in virulence and fitness might exist in the PDE and PFG domains of VP2. To test this, five amino acid changes selected by sequence comparison of the PDE and PFG domains of VP2 were introduced individually using a reverse genetics system into the virulent strain (rGx-F9VP2). Then reverse mutations of the selected residues 249 and 256 were introduced individually into the attenuated strain (rGt). Seven modified viruses were generated and evaluated in vitro (CEF cells) and in vivo (SPF chicken). For residue 249, Q249R could elevate in vitro and reduce in vivo the replication of rGx-F9VP2 while R249Q could reduce in vitro and elevate in vivo the replication of rGt; meanwhile Q249R reduced the virulence of rGx-F9VP2 while R249Q increased the virulence of rGt, which indicated that residue 249 significantly contributed to the replication and virulence of IBDV. For residue 256, I256V could elevate in vitro and reduce in vivo the replication of rGx-F9VP2 while V256I could reduce in vitro but didn’t change in vivo the replication of rGt; although V256I didn’t increase the virulence of rGt, I256V obviously reduced the virulence of virulent IBDV. The present results demonstrate for the first time, to different extent, residues 249 and 256 of VP2 are involved in the replication efficiency and virulence of IBDV; this is not only beneficial to further understanding of pathogenic mechanism but also to the design of newly tailored vaccines against IBDV.

show abstract

“…The assay to determine IBDV neutralization by mice and chickens sera was performed essentially as described by Schröder et al ., 2000 [78]. Virus strain D78 was applied.…”

Section: Methodsmentioning

confidence: 99%

Protective Vaccination against Infectious Bursal Disease Virus with Whole Recombinant Kluyveromyces lactis Yeast Expressing the Viral VP2 Subunit

et al. 2012

Self Cite

View full text Add to dashboard Cite

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.

show abstract

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

Cited by 29 publications

References 28 publications

Different Domains of the RNA Polymerase of Infectious Bursal Disease Virus Contribute to Virulence

Different Domains of the RNA Polymerase of Infectious Bursal Disease Virus Contribute to Virulence

Mutations of Residues 249 and 256 in VP2 Are Involved in the Replication and Virulence of Infectious Bursal Disease Virus

Protective Vaccination against Infectious Bursal Disease Virus with Whole Recombinant Kluyveromyces lactis Yeast Expressing the Viral VP2 Subunit

Contact Info

Product

Resources

About