Extensive antigenic changes in an atypical isolate of very virulent infectious bursal disease virus and experimental clinical control of this virus with an antigenically classical live vaccine

Eterradossi, Nicolas; Gauthier, C; Reda, I. M.; Comte, Sylvain; Rivallan, G.; Toquin, D.; Boisséson, Claire de; Lamande, J.; Jestin, Véronique; Morin, Yannick; Cazaban, Christophe; Borne, Pierre-marie

doi:10.1080/03079450410001724049

Cited by 26 publications

(8 citation statements)

References 37 publications

(53 reference statements)

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“…However, since most of the recombinant viruses studied here replicated to similar extents in the BF irrespective of their VP2 sequences, the hypothesis that differences in pathogenicity such as those observed here stem from different interactions with the IBDV receptor seems somewhat remote. Interestingly, vvIBDV strain 99323, which exhibits the A321T change, proved as pathogenic as French vvIBDV reference isolate 89163 under the same experimental conditions as those used here (52). Comparison of the molecular structures of the V and T residues suggests a critical role for the methyl group found at the ␥ position in the V321 residue, which would result in low pathogenicity, whereas a hydroxyl group, such as that found at the ␥ position in the T321 residue, would not.…”

Section: Discussionmentioning

confidence: 49%

“…The parent virus 94432 and its molecular copy mc94432 were characterized antigenically by using an antigen capture enzyme-linked immunosorbent assay (AC-ELISA) as described previously. This test is based on a panel of eight IBDV-specific neutralizing monoclonal antibodies (Mabs) that detected at least six epitopes located in the VP2 hypervariable domain (43,46,52).…”

Section: Ethics Statementmentioning

confidence: 99%

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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: 49%

Section: Ethics Statementmentioning

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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“…However, some variation in the mortality induced by mc88180 was observed in our three animal experiments, as the mc88180-induced mortality ranged 5 to 27% (no statistically significant difference according to the Chi-squared test). Although mortality in the first experiment (27%) did not differ significantly from that induced by the 89163 vvIBDV control virus (30%), the percent mortality observed in subsequent experiments was lower than would have been expected in our experimental model for a typical vvIBDV [44], [47], [48]. Whether some genetic specificities of 88180 might be associated with a reduced pathogenicity as compared with vvIBDV will be discussed below.…”

Section: Discussionmentioning

confidence: 67%

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

et al. 2012

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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.

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“…The vvIBDV virulence is partly determined by its VP1 gene (Boot et al, 2000(Boot et al, , 2005, but vvIBDVs are antigenically similar to classic IBDVs and can be controlled with currently available IBDV vaccines (Tsukamoto et al, 1995;Eterradossi et al, 2004). The vvIBDVs are present in Europe, Asia, Africa and South America, but have not yet been detected in the USA, Canada, Australia and New Zealand (van den Berg et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Genotyping of Canadian field strains of infectious bursal disease virus

et al. 2007

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For this retrospective study, infectious bursal disease virus (IBDV) was detected in 134 bursal samples that originated from flocks with conditions such as airsacculitis, tracheitis, pneumonia, septicaemia, inclusion body hepatitis, coccidiosis, and/or a history of production problems without overt clinical symptoms. Samples were from seven Canadian provinces: Ontario, Quebec, Manitoba, British Columbia, Nova Scotia, Alberta, and Newfoundland and Labrador. Viral RNA was identified in bursae with moderate to severe and acute to chronic bursal damage. The ages of the flocks from which samples were collected ranged from 3 to 63 days. Following reverse transcriptase-polymerase chain reaction the nucleotide sequence of the VP2 hypervariable region was determined and compared with sequences available in GenBank. The most common Canadian IBDV field strains were North-American variant viruses. Forty-four viruses were highly related (97.5% to 100.0%) to the US IBDV strain NC171. Moreover, 16 field viruses whose VP2 sequences were 99.2% to 100% identical to the South African 05SA8 IBDV strain appeared closely related to the NC171 group. Delaware E-related field viruses, 98.3% to 100.0% identical to the prototype virus, were identified in 33 samples. Thirty-four Canadian IBDVs showed the highest identity, 94.2% to 98.3%, to US IBDV strain 586. Five samples contained vaccine-related viruses, while two field strains showed the best match to Del A (United States) and IBDV strains SP_04_02 (Spain). Very virulent IBDVs were not detected in Canada.

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Extensive antigenic changes in an atypical isolate of very virulent infectious bursal disease virus and experimental clinical control of this virus with an antigenically classical live vaccine

Cited by 26 publications

References 37 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

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

Genotyping of Canadian field strains of infectious bursal disease virus

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