The enhanced virulence of very virulent infectious bursal disease virus is partly determined by its B-segment

Boot, Hein J.; Hoekman, A.J.W.; Gielkens, A. L. J.

doi:10.1007/s00705-004-0405-9

Cited by 53 publications

(48 citation statements)

References 17 publications

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“…A number of reports have demonstrated the drastic effects of mutations of VP2 residues on attenuation of the virulence of vvIBDV (3,43); these residues were proposed to be related to the protein's receptor binding efficiency (5), but they are not the sole determinants of virulence (2). On the other hand, VP1 was also demonstrated to be a determinant of virulence in vivo, possibly by altering the replication efficiency (1,26). A recent study reported the isolation of a naturally reassorted IBDV with genome segment A of very virulent origin but genome segment B of non-very virulent origin; this isolate showed significantly reduced pathogenicity compared with typical vvIBDVs (25), demonstrating that the determinants on genome segment A may not be enough to induce the hypervirulence of typical vvIBDVs.…”

Section: Discussionmentioning

confidence: 99%

Phylogenetic Analysis Reveals a Correlation between the Expansion of Very Virulent Infectious Bursal Disease Virus and Reassortment of Its Genome Segment B

Hon

Lam

Drummond

et al. 2006

J Virol

101

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Infectious bursal disease virus (IBDV) is a birnavirus causing immunosuppressive disease in chickens.Emergence of the very virulent form of IBDV (vvIBDV) in the late 1980s dramatically changed the epidemiology of the disease. In this study, we investigated the phylogenetic origins of its genome segments and estimated the time of emergence of their most recent common ancestors. Moreover, with recently developed coalescence techniques, we reconstructed the past population dynamics of vvIBDV and timed the onset of its expansion to the late 1980s. Our analysis suggests that genome segment A of vvIBDV emerged at least 20 years before its expansion, which argues against the hypothesis that mutation of genome segment A is the major contributing factor in the emergence and expansion of vvIBDV. Alternatively, the phylogeny of genome segment B suggests a possible reassortment event estimated to have taken place around the mid-1980s, which seems to coincide with its expansion within approximately 5 years. We therefore hypothesize that the reassortment of genome segment B initiated vvIBDV expansion in the late 1980s, possibly by enhancing the virulence of the virus synergistically with its existing genome segment A. This report reveals the possible mechanisms leading to the emergence and expansion of vvIBDV, which would certainly provide insights into the scope of surveillance and prevention efforts regarding the disease.Infectious bursal disease (IBD) is an immunosuppressive disease of young chickens that causes considerable economic loss to the poultry industry worldwide. The causative agent of IBD is a bisegmented, double-stranded RNA virus of the Birnaviridae family named IBD virus (IBDV). IBD was firstly reported in 1957 in broilers of the Delmarva Peninsula of the United States. It had spread rapidly throughout the United States by 1965 but was effectively controlled by vaccinations in the mid-1970s (23). In 1986, vaccination failures were reported and IBDV isolates with enhanced virulence were identified and characterized (18). These new isolates, named very virulent IBDV (vvIBDV), were then described by Chettle and coworkers (4) as the causative agents of the first reported cases of severe and acute IBD in Europe. These very virulent strains have rapidly spread all over Asia and other parts of the world (11) in an explosive manner (42), following their introduction into Japan in the early 1990s (30).The epidemiological event leading to the emergence and expansion of vvIBDV is an open question. Phylogenetic analyses have revealed independent evolutionary histories of the two genome segments (17, 44), suggesting that a reassortment event may have played a role in the emergence of vvIBDV. Previous reports suggested that both the major capsid protein (VP2) and the RNA-dependent RNA polymerase (VP1), which are located on genome segments A and B, respectively, contribute to the virulence of IBDV (1-3, 26, 43). Questions have been raised regarding the phylogenetic origins and roles of the unique mutations of the two genome...

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Section: Discussionmentioning

confidence: 99%

Phylogenetic Analysis Reveals a Correlation between the Expansion of Very Virulent Infectious Bursal Disease Virus and Reassortment of Its Genome Segment B

Hon

Lam

Drummond

et al. 2006

J Virol

101

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“…The resulting viruses proved to be attenuated for chickens (34,35), but reversion mutations were observed upon passage in chickens and could restore virulence (36). VP2 is, however, unlikely to be the only factor for virulence: laboratory-engineered reassortant viruses derived from vvIBDV exhibited delayed replication in the bursa (37) or failed to induce morbidity and mortality (31) unless they also had a typical vvIBDV-related segment B. This observation is consistent with the phylogeny-based hypothesis that both genome segments may be involved in the emergence of vvIBDV (38,39).…”

Section: Nfectious Bursal Disease Virus (Ibdv) Of Chickens (Gallus mentioning

confidence: 99%

Both Genome Segments Contribute to the Pathogenicity of Very Virulent Infectious Bursal Disease Virus

Escaffre

Nouën

Amelot

et al. 2013

J Virol

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f Infectious bursal disease virus (IBDV) causes an economically significant disease of chickens worldwide. Very virulent IBDV (vvIBDV) strains have emerged and induce as much as 60% mortality. The molecular basis for vvIBDV pathogenicity is not understood, and the relative contributions of the two genome segments, A and B, to this phenomenon are not known. Isolate 94432 has been shown previously to be genetically related to vvIBDVs but exhibits atypical antigenicity and does not cause mortality. Here the full-length genome of 94432 was determined, and a reverse genetics system was established. The molecular clone was rescued and exhibited the same antigenicity and reduced pathogenicity as isolate 94432. Genetically modified viruses derived from 94432, whose vvIBDV consensus nucleotide sequence was restored in segment A and/or B, were produced, and their pathogenicity was assessed in specific-pathogen-free chickens. We found that a valine (position 321) that modifies the most exposed part of the capsid protein VP2 critically modified the antigenicity and partially reduced the pathogenicity of 94432. However, a threonine (position 276) located in the finger domain of the virus polymerase (VP1) contributed even more significantly to attenuation. This threonine is partially exposed in a hydrophobic groove on the VP1 surface, suggesting possible interactions between VP1 and another, as yet unidentified molecule at this amino acid position. The restored vvIBDV-like pathogenicity was associated with increased replication and lesions in the thymus and spleen. These results demonstrate that both genome segments influence vvIBDV pathogenicity and may provide new targets for the attenuation of vvIBDVs.

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“…Molecular characterization of IBDV has been based mainly on the analysis of the sequence of the variable region of VP2. However, there is evidence suggesting that VP2 is not the only protein responsible for pathogenicity of IBDV; other viral proteins may contribute to enhance the pathogenicity, particularly VP1 [30,36]. In addition to this, it has been shown that different vvIBDVs form a tight cluster, quite separate from other IBDV strains, when segment B is analyzed, which justifies the characterization of IBDV strains based on both genomic segments [37], particularly because it has been noted that it is possible for IBDV to undergo genetic reassortment, which can play an important role in the evolution of these viruses [38][39][40].…”

Section: Introductionmentioning

confidence: 99%

Molecular characterization of infectious bursal disease virus (IBDV) isolated in Argentina indicates a regional lineage

Vera

Craig²,

Olivera³

et al. 2015

Arch Virol

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In Argentina, classical vaccines are used to control infectious bursal disease virus (IBDV); however, outbreaks of IBDV are frequently observed. This could be due to failures in the vaccination programs or to the emergence of new strains, which would be able to break through the protection given by vaccines. Hence, genetic characterization of the viruses responsible for the outbreaks that occurred in recent years is crucial for the evaluation of the control programs and the understanding of the epidemiology and evolution of IBDV. In this study, we characterized 51 field samples collected in Argentina (previously identified as IBDV positive) through the analysis of previously identified apomorphic sequences. Phylogenetic analysis of regVP2 showed that 42 samples formed a unique cluster (Argentinean lineage), seven samples were typical classical strains (one of them was a vaccine strain), and two belonged to the very virulent lineage (vvIBDV). Interestingly, when the analysis was performed on the regVP1 sequences, the field samples segregated similarly to regVP2; thus, we observed no evidence of a reassortment event in the Argentinean samples. Amino acid sequence analysis of regVP2 showed a particular pattern of residues in the Argentinean lineage, particularly the presence of T272, P289 and F296, which had not been reported before as signature sequences for any IBDV phenotype. Notably, the residue S254, characteristic of the antigenic variant, was not present in any of the Argentinean samples.

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The enhanced virulence of very virulent infectious bursal disease virus is partly determined by its B-segment

Cited by 53 publications

References 17 publications

Phylogenetic Analysis Reveals a Correlation between the Expansion of Very Virulent Infectious Bursal Disease Virus and Reassortment of Its Genome Segment B

Phylogenetic Analysis Reveals a Correlation between the Expansion of Very Virulent Infectious Bursal Disease Virus and Reassortment of Its Genome Segment B

Both Genome Segments Contribute to the Pathogenicity of Very Virulent Infectious Bursal Disease Virus

Molecular characterization of infectious bursal disease virus (IBDV) isolated in Argentina indicates a regional lineage

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