Naturally occurring mutations at residues 253 and 284 in VP2 contribute to the cell tropism and virulence of very virulent infectious bursal disease virus

Qi, Xiaole; Gao, Honglei; Gao, Yulong; Qin, Liting; Wang, Yongqiang; Gao, Li; Wang, Xiaomei

doi:10.1016/j.antiviral.2009.09.006

Cited by 58 publications

(51 citation statements)

References 39 publications

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“…Indeed, the VP2-encoding region of a typical vvIBDV, expressed in the genetic context of a mildly virulent cell culture-adapted IBDV recipient strain, conferred the ability to induce severe bursal lesions (31). In addition, the alteration of VP2 amino acids (aa) 253, 279, and/or 284 of a vvIBDV strain by reverse genetics conferred adaptation to chicken embryo fibroblasts (CEF) (32)(33)(34). 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).…”

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

confidence: 99%

“…In addition, the alteration of VP2 amino acids (aa) 253, 279, and/or 284 of a vvIBDV strain by reverse genetics conferred adaptation to chicken embryo fibroblasts (CEF) (32)(33)(34). 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.…”

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

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

confidence: 99%

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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“…In terms of disease control and early warning, it is important to fully understand the gene or residue function. Since the development of reverse genetics, the role of VP2 in replication or virulence has attracted much attention (Brandt et al, 2001;Li et al, 2015;Qi et al, 2009Qi et al, , 2013van Loon et al, 2002). However, the precise molecular determinants are still somewhat unclear.…”

Section: Discussionmentioning

confidence: 99%

“…The tower-like P domain contains four loops, P BC , P HI , P DE , and P FG . It has been reported that the P DE and P FG domains are responsible for cell-tropism and virulence (Brandt et al, 2001;Qi et al, 2009Qi et al, , 2013van Loon et al, 2002). The other two loops, P BC and P HI , are also located at the tip of the VP2 spike; however, their roles in viral replication and virulence are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

“…Previously, a moderately virulent IBDV strain (rGx-F9VP2) and an attenuated strain (rGt) were rescued, providing a good model system for studying the viral replication and virulence of IBDV (Qi et al, 2007(Qi et al, , 2009(Qi et al, , 2013). In the current study, specific amino acid mutations in the P BC and P HI domains of VP2 were introduced into the backbone of the virulent (rGx-F9VP2) and attenuated (rGt) strains in order to evaluate the roles of these amino acid changes in replication and virulence.…”

Section: Introductionmentioning

confidence: 99%

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A single mutation in the PBC loop of VP2 is involved in the in vitro replication of infectious bursal disease virus

Gao

et al. 2016

Sci. China Life Sci.

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To test whether amino acid mutations in the P BC and P HI loops of VP2 are involved in the replication and virulence of infectious bursal disease virus (IBDV), a pair of viruses, namely the moderately virulent IBDV (rGx-F9VP2) and the attenuated strain (rGt), were used. Residue mutations A222P (P BC ) and S330R (P HI ), selected by sequence comparison, were introduced individually into rGx-F9VP2 by using a reverse genetics system. In addition, the reverse mutation of either P222A or R330S was introduced into rGt. The four modified viruses were then rescued and evaluated in vitro (CEF cells) and in vivo (SPF chickens). Results showed that A222P elevated the replication efficiency of rGx-F9VP2 while P222A reduced that of rGt in CEF cells. A mutation at residue 330 did not alter IBDV replication. In addition, animal experiments showed that a single mutation at either residue 222 or 330 did not significantly influence the virulence of IBDV. In conclusion, residue 222 in P BC of VP2 is involved in the replication efficiency of IBDV in vitro but does not affect its virulence in vivo, further facilitating our understanding of the gene-function of IBDV. infectious bursal disease virus (IBDV), VP2, P BC , replicationCitation:

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Infectious Bursal Disease Virus

Gómez

Lucero

Richetta

et al. 2018

Prospects of Plant-Based Vaccines in Veterinary Medicine

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Naturally occurring mutations at residues 253 and 284 in VP2 contribute to the cell tropism and virulence of very virulent infectious bursal disease virus

Cited by 58 publications

References 39 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

A single mutation in the PBC loop of VP2 is involved in the in vitro replication of infectious bursal disease virus

Infectious Bursal Disease Virus

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