Genetic reassortment of infectious bursal disease virus in nature

Wei, Yongwei; Lǐ, Jiànróng; Zheng, Jie; Xu, Hong; Li, Long; Liang, Yu

doi:10.1016/j.bbrc.2006.09.040

Cited by 84 publications

(56 citation statements)

References 42 publications

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“…In one study, a recombinant virus with segment A derived from the cell culture-adapted strain CEF94 and segment B derived from the vvIBDV strain D6948 failed to induce mortality (31). However, in another study, two natural reassortant strains with similar genetic makeups induced 20 to 30% mortality (64,65). The current study demonstrates that both genomic segments of 94432, both of which are phylogenetically related to those of vvIBDVs, do contribute to pathogenicity.…”

Section: Discussionmentioning

confidence: 55%

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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Section: Discussionmentioning

confidence: 55%

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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“…The results further suggested that segment A of GX-NN-L was derived from a vvIBDV strain and segment B was derived from an attenuated strain (12). Alignment analysis results indicated that VP5 of GX-NN-L had a four-amino-acid (MLSL) deletion in the N-terminal extension which met vvIBDV characteristics (11). There were four unique nucleotide substitutions (E18K, A51T, T135I, and W137R) in VP5 of GX-NN-L compared to that of other vvIBDV isolates, differences which might be responsible for the variability of the GX-NN-L isolate in virulence and adaptability (1,8).…”

Section: Nfectious Bursal Disease Virus (Ibdv) Belongs To the Familymentioning

confidence: 87%

“…The genome of IBDV is a bisegmented doublestranded RNA consisting of 2 segments (A and B); segment A encodes VP5 and polyprotein (VP2-VP4-VP3), while segment B encodes VP1 protein (5). The coinfection with very virulent IBDV (vvIBDV) and attenuated IBDV strains led to exchange of the double-stranded genomic RNA segments to generate new reassortant viruses (2,3,11).…”

Section: Nfectious Bursal Disease Virus (Ibdv) Belongs To the Familymentioning

confidence: 99%

Complete Genome Sequence Analysis of a Natural Reassortant Infectious Bursal Disease Virus in China

Chen

Liu

Zhang

et al. 2012

J Virol

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A novel isolate of infectious bursal disease virus (IBDV) was designated GX-NN-L. The GX-NN-L IBDV was a very virulent infectious bursal disease virus (vvIBDV) isolated from broiler flocks in Guangxi province, China, in 2011. The GX-NN-L IBDV caused high mortality, immunosuppression, low weight gain, and bursal atrophy in commercial broilers. Here, we report the complete genome sequence of the GX-NN-L IBDV, a reassortment strain with segments A and B derived from very virulent strains and attenuated IBDV, respectively. These findings from this study provide additional insights into the genetic exchange between attenuated and very virulent strains of IBDV and continuous monitoring of the spread of the virus in chicken.

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“…The three previous cvVP2 IBDV samples were also classified as cv strains using the VP1 aa sequences. In thirteen of the samples identified as vvVP2, all of the four common and characteristic aa substitutions of the vv strains within the VP1 fragment were found ( (26,27). It could be another explanation for the origin of the Br/03/DR sample.…”

Section: Resultsmentioning

confidence: 99%

Partial VP1 sequencing of Brazilian infectious bursal disease virus strains

Fernandes¹,

Simoni²,

Harakava³

et al. 2012

Braz. J. Microbiol.

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Infectious bursal disease virus (IBDV) is classified according to the antigenicity and virulence into classical virulent (cv), very virulent (vv), and antigenic variant strains. The molecular basis for the IBDV antigenic variation is well established and is associated to the capsid protein, VP2 (gene VP2 of segment A), whereas both VP2 and the RNA-dependent RNA polymerase, VP1 (gene VP1 of segment B), have been correlated with the virulence. In this study, seventeen Brazilian IBDV samples previously characterized by the VP2 gene as cv (three) and vv (fourteen) strains were genetically and molecularly analyzed for their VP1 gene.All of the strains kept with the same cv or vv classification except one sample, Br/03/DR. This sample was classified as vv by its VP2 gene, but it was most closely related to the cv strains by its VP1 partial sequence and phylogeny. Studies on the phylogeny of VP1 have suggested a possible reassortment event that originated the vvVP1. In this case, the sample carrying vvVP2 and cvVP1 could be a descendant of IBDV ancestors prior to the reassortment of vvVP1; alternatively, it could be the result of a genetic exchange between the segments of different strains or with a live attenuated vaccine. Nevertheless, this is the first report of natural genetic reassortment of IBDV in Brazil.

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Genetic reassortment of infectious bursal disease virus in nature

Cited by 84 publications

References 42 publications

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

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

Complete Genome Sequence Analysis of a Natural Reassortant Infectious Bursal Disease Virus in China

Partial VP1 sequencing of Brazilian infectious bursal disease virus strains

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