The genome segment B encoding the RNA-dependent RNA polymerase protein VP1 of very virulent infectious bursal disease virus (IBDV) is phylogenetically distinct from that of all other IBDV strains

Islam, Md. Rafiqul; Zierenberg, Kati; Müller, Hermann

doi:10.1007/s007050170018

Cited by 53 publications

(44 citation statements)

References 36 publications

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“…In contrast, in the BMCMC phylogeny of VP1, the vvIBDV clade (vvVP1) was excluded from the lineage containing all other serotype I and II IBDV strains (0.87 BP support) (Fig. 1B), revealing an independent phylogenetic origin of vvVP1 that agreed with previous reports (17). The high BP support (0.99) of the monophyletic IBDV VP1 lineage in the birnavirus VP1 phylogeny suggests that vvVP1 may have an avian origin that shares the TMRCA with the other IBDV strains.…”

Section: Resultssupporting

confidence: 90%

“…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).…”

Section: Infectious Bursal Disease Virus (Ibdv) Is a Birnavirus Causimentioning

confidence: 99%

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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: Resultssupporting

confidence: 90%

Section: Infectious Bursal Disease Virus (Ibdv) Is a Birnavirus Causimentioning

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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“…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). Recently, this hypothesis was substantiated by the isolation of three naturally occurring segment B-reassorted vvIBDV isolates, all with reduced pathogenicity in chickens (40,41).…”

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

confidence: 58%

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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“…Changes in the variable region of VP2 should be considered evolutionary rather than virulence markers and the potential for new and antigenically divergent lineages of vvIBDVs in the future should not be excluded. Sequence comparisons between pathogenic and non-pathogenic serotype 1 strains have shown differences throughout the genome (Brown & Skinner, 1996;Yamaguchi et al, 1997;Pitcovski et al, 1998;Yehuda et al, 1999;Islam et al, 2001) indicating that different areas of the genome might contribute to virulence. In order to investigate this further, full-length sequencing and comparison of the genomes of the nine investigated strains is in progress.…”

Section: Discussionmentioning

confidence: 99%

Assessment of genetic, antigenic and pathotypic criteria for the characterization of IBDV strains

Berg

Morales

Eterradossi³

et al. 2004

Avian Pathology

Self Cite

127

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The aim of this work was the selection and comparison of representative infectious bursal disease virus (IBDV) strains. Nine strains of IBDV, isolated at different times and from different geographic regions of Europe and China, were characterized. Batches of all strains were prepared following standardized protocols and checked for the absence of contaminating viruses. Criteria used for their characterization were: (i) the nucleotide sequence of the VP2 variable region, (ii) binding to a panel of neutralizing monoclonal antibodies in antigen capture enzyme-linked immunosorbent assays, and (iii) virulence in specific pathogen free chickens after infection with a standardized number of median embryo infective doses. Based on the first two criteria, two of nine strains were classified as classical virulent (cv) IBDV (F52/70, Cu-1wt), and five as very virulent (vv) IBDV (849VB, 96108, HK46, GX, Harbin). Remarkably, although a clear-cut difference was demonstrable between European cvIBDV (F52/70 and Cu-1wt) and vvIBDV (849VB and 96108) strains, there was a continuum in the pathogenicity of Chinese vvIBDVs. Our results indicate the probable existence of differences in virulence within IBDV lineages determined on the basis of antigenic typing using monoclonal antibodies and the alignment of the VP2 sequences. This indicates limitations in the analysis of IBDV pathotypes based on the VP2 variable region and emphasizes that these criteria may not be sufficient for the classification of IBDV strains.

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The genome segment B encoding the RNA-dependent RNA polymerase protein VP1 of very virulent infectious bursal disease virus (IBDV) is phylogenetically distinct from that of all other IBDV strains

Cited by 53 publications

References 36 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

Assessment of genetic, antigenic and pathotypic criteria for the characterization of IBDV strains

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