Identification and pathogenicity of a natural reassortant between a very virulent serotype 1 infectious bursal disease virus (IBDV) and a serotype 2 IBDV

Jackwood, Daral J.; Sommer-Wagner, Susan E.; Crossley, Beate; Stoute, Simone; Woolcock, P. R.; Charlton, B. R.

doi:10.1016/j.virol.2011.08.023

Cited by 68 publications

(60 citation statements)

References 43 publications

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“…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). Another recent experimental study based on reverse genetics demonstrated that several domains of the IBDV polymerase may contribute to virulence (42).…”

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

confidence: 84%

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

confidence: 84%

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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“…16 These primers amplify a 778-bp region of the serotype 2 VP2 gene from nucleotides 686-1,463 and do not amplify genome segment A of serotype 1 IBDV. The amplified serotype 2 segment A product was detected using probe f FAM-5'-GTCGCAA CTCATCCCAAGT-3'.…”

Section: Real-time Rt-pcr Amplificationmentioning

confidence: 99%

“…16 The amplified segment B product was detected using probe f FAM-5'-TACTCAAGCAGATGAT-3'. The cDNA synthesis, pre-denaturation, and PCR conditions were as described previously.…”

Section: Real-time Rt-pcr Amplificationmentioning

confidence: 99%

Pathogenicity associated with coinfection with very virulent infectious bursal disease and Infectious bursal disease virus strains endemic in the United States

et al. 2013

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The pathogenicity induced by co-challenge with the rB strain of very virulent Infectious bursal disease virus (vvIBDV) and IBDV pathotypes endemic in the United States was evaluated in specific pathogen-free chickens. Four- and 6-week-old birds were simultaneously challenged with a 10(5) 50% egg infectious dose (EID50) of rB mixed with a 10(5) EID50 of one of the following viruses: standard classic (STC), subclinical variant (Del-E), subclinical variant (T1), or avirulent serotype 2 (OH). Each challenge group consisted of 5 chickens. The severity of disease was assessed by comparing the 5-day mortality rates, bursal lesions (mean bursal lesion scores), and mean bursal-to-body weight ratios in each of the challenged groups. A mortality of 100% (10/10 and 5/5) was observed in birds inoculated with only the vvIBDV (rB) strain at 4 weeks and 6 weeks of age, respectively. Although the sample sizes were low, a significant reduction in mortality and severity of disease, based on mean bursal lesion scores, was observed in groups co-challenged with rB and the less virulent pathotypes Del-E, T1, or OH at 4 weeks of age. Co-challenge with rB and the antigenically similar STC strain did not result in a significant decrease in mortality compared to challenge with the pathogenic rB strain at 4 weeks of age, but a significant reduction in the mean bursa lesion score was observed. At 6 weeks of age, a significant decrease in mortality and mean bursa lesion score was observed in the rB groups co-challenged with STC, Del-E, or T1 but not OH.

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“…Glutamic acid is characterized by negatively charged (acidic) R group, whereas, the R group in alanine is non polar (hydrophobic). It is probable that this change from negative charge to non-polar may modify the protein folding or the interaction with other molecules that may change the topography of the neutralizing epitopes that may lead to vaccination failure (Jackwood et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Sequence analysis of VP2 hypervariable region of the field isolates of infectious bursal disease viruses from southern region of India

Raja¹,

Senthilkumar²,

Priyadarshini³

et al. 2018

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Infectious bursal disease virus isolates obtained from southern parts of India were subjected to comparative sequencing and phylogenetic analysis of 743bp hypervariable region of VP2. The sequence analysis showed that among eight isolates, only HY12 showed the characteristic conserved amino acid residues at 256I, 294I, and 299S of vvIBDV. Six isolates BGE14, PY12, NKL14, VCN14, RPM14 and EDE14 had conserved amino acid residues at 256I and 299S, whereas at residue 294, isoleucine was substituted by valine. The remaining isolate MB11 had leucine at residue 294 and asparagine at residue 299 similar to classical strain 52/70. The serine-rich heptapeptide sequence SWSASGS adjacent to the second hydrophilic region was conserved in all seven Indian IBDV isolates except isolate MB11. Conservation of this sequence was earlier reported to be an indication of a virus isolate being pathogenic in nature. The reported heptapeptide sequence of the classical strain is 'SWSARGS'. In the present study, 'SWSARGS' heptapeptide sequence was observed in MB11 isolate. The pathogenicity trials conducted with these isolates further confirmed the genome analysis in classification. This study further reveals that the circulating IBDV strains in India could be diverse in nature.

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Identification and pathogenicity of a natural reassortant between a very virulent serotype 1 infectious bursal disease virus (IBDV) and a serotype 2 IBDV

Cited by 68 publications

References 43 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

Pathogenicity associated with coinfection with very virulent infectious bursal disease and Infectious bursal disease virus strains endemic in the United States

Sequence analysis of VP2 hypervariable region of the field isolates of infectious bursal disease viruses from southern region of India

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