Loss of virulence in a small plaque mutant of the infectious bursal disease virus

Cursiefen, Dagmar; Käufer, I; Becht, H.

doi:10.1007/bf01317893

Cited by 33 publications

(15 citation statements)

References 9 publications

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“…In isolated B lymphocytes IBDV replication is initiated as soon as 90 min after infection (Mü ller & Becht, 1982) and viral progeny is formed after 6 to 8 h (Cursiefen et al, 1979). These data indicate that several rounds of IBDV replication take place in the bursa of infected chickens, considerably increasing the risk of reversion.…”

Section: Discussionmentioning

confidence: 91%

Reversion of molecularly engineered, partially attenuated, very virulent infectious bursal disease virus during infection of commercial chickens

Raue

Islam

et al. 2004

Avian Pathology

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A molecularly cloned, tissue culture-adapted infectious bursal disease virus (BD-3tc) was generated from a very virulent strain by the reverse genetics approach following site-directed mutagenesis (Q253H and A284T in VP2). The pathogenicity of BD-3tc was tested in commercial chickens. The wild-type strain (BD-3wt) and the molecularly cloned parental strain (BD-3mc) were included for comparison. The subclinical course of the disease, with delayed and milder pathological lesions followed by quick follicular regeneration in the bursa of Fabricius in BD-3tc-inoculated birds, suggested that these amino acid substitutions made BD-3tc partially attenuated. However, severe bursa atrophy was observed at 14 days after inoculation. Reverse transcription-polymerase chain reaction coupled with restriction enzyme analysis revealed that both point mutations in BD-3tc had reverted 14 days after inoculation. Further investigations demonstrated that the codon for amino acid at position 284 had already reverted to the wild-type phenotype (T284A) 3 days after inoculation.

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Section: Discussionmentioning

confidence: 91%

Reversion of molecularly engineered, partially attenuated, very virulent infectious bursal disease virus during infection of commercial chickens

Raue

Islam

et al. 2004

Avian Pathology

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“…It is unlikely that the VP 4 sequences had any role in protection since VP 4 is only a minor component of viral capsids [25]. Protection against mortality was achieved despite the absence of detectable circulating IBDV antibodies, the presence of which correlates with protection [14]. Failure to stimulate high levels of humoral antibody in chickens to genes inserted in FPV has been shown previously [8,9], using the present FPV vector to express the F or HN genes of NDV.…”

Section: Discussionmentioning

confidence: 93%

A recombinant fowlpox virus that expresses the VP2 antigen of infectious bursal disease virus induces protection against mortality caused by the virus

Bayliss

Peters

Cook

et al. 1991

Archives of Virology

101

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The coding sequences of VP2 from a virulent strain, 52/70, of infectious bursal disease virus (IBDV) were excised from a cDNA clone and inserted into a fowlpox plasmid insertion vector. The resulting plasmid, pIBD 1, was used to construct a recombinant fowlpox virus, fpIBD 1, which expressed VP 2 as a beta-galactosidase fusion protein. Chickens vaccinated with fpIBD 1 at 1 and 14 days of age, were challenged at 28 days with either IBDV strain 52/70 or the highly virulent strain CS 89. These chickens were protected against mortality, but not against damage to the bursa of Fabricius. The protection achieved by the use of fpIBD 1 shows that VP 2 is a host protective antigen.

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“…Although the last few years have witnessed major progress in the understanding of IBDV molecular and structural biology aspects, key issues concerning the virus replication programme remain poorly characterized. This lack of information is exemplified by the fact that, although the tropism of IBDV for bursal B-lymphocyte populations was first described and characterized extensively over 25 years ago (Becht, 1980;Kibenge et al, 1988), the discovery of the mechanism(s) governing this phenomenon still represents the holy grail of IBDV biology.Propagation of IBDV field isolates in tissue culture requires previous adaptation involving serial virus passage, a process that invariably leads to the introduction of mutations at specific residues on the VP2 capsid polypeptide, as well as a significant reduction of virus virulence (Cursiefen et al, 1979; Hassan et al, 1996;Lange et al, 1987; Yamaguchi et al, 1996a, b). This phenomenon constitutes a major obstacle to characterizing the interaction of pathogenic IBDV strains with susceptible host cells.…”

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confidence: 99%

Infectious bursal disease virus persistently infects bursal B-lymphoid DT40 cells

Delgui

González

Rodrı́guez

2009

Journal of General Virology

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Infectious bursal disease virus (IBDV), an important avian pathogen, exhibits a specific tropism for immature B-lymphocyte populations. We have investigated the ability of IBDV to replicate in chicken B-lymphoid DT40 cells, a tumour cell line derived from the bursa of Fabricius of a chicken infected with avian leukosis virus. Our results show that IBDV persistently infects DT40 cells. Establishment of the persistent infection is associated with an extensive remodelling of the hypervariable region of the VP2 capsid polypeptide, accumulating 14 amino acid changes during the first 60 days of the persistent infection. The amino acid sequence of the non-structural VP5 polypeptide, involved in virus dissemination, is not altered during the persistent infection. Results described in this report constitute the first demonstration of the ability of IBDV to establish a persistent infection in vitro.Infectious bursal disease virus (IBDV), an avian pathogen responsible for a highly contagious immunosuppressive disease, is the best-characterized member of the family Birnaviridae. Birnaviruses are naked, icosahedral viruses with bipartite, double-stranded RNA genomes (Dobos et al., 1979). Although the last few years have witnessed major progress in the understanding of IBDV molecular and structural biology aspects, key issues concerning the virus replication programme remain poorly characterized. This lack of information is exemplified by the fact that, although the tropism of IBDV for bursal B-lymphocyte populations was first described and characterized extensively over 25 years ago (Becht, 1980;Kibenge et al., 1988), the discovery of the mechanism(s) governing this phenomenon still represents the holy grail of IBDV biology.Propagation of IBDV field isolates in tissue culture requires previous adaptation involving serial virus passage, a process that invariably leads to the introduction of mutations at specific residues on the VP2 capsid polypeptide, as well as a significant reduction of virus virulence (Cursiefen et al., 1979; Hassan et al., 1996;Lange et al., 1987; Yamaguchi et al., 1996a, b). This phenomenon constitutes a major obstacle to characterizing the interaction of pathogenic IBDV strains with susceptible host cells.In a recent report, Terasaki et al. (2008) showed that very virulent IBDV isolates can be grown directly in chicken lymphoid DT40 tumour cells infected persistently with avian leukosis virus (ALV) (Baba et al., 1985), without the requirement for a preliminary adaptation process. Most importantly, serial passage in this cell line does not result in the incorporation of mutations at the specific VP2 residues. Additionally, DT40 cells show an extremely high frequency of homologous recombination (Buerstedde & Takeda, 1991). This property has been exploited widely for the generation of derivative cell lines in which selected target genes are inactivated (Winding & Berchtold, 2001). Accordingly, DT40 cells appear to be an excellent candidate system to undertake a systematic analysis aimed at determining the ...

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Loss of virulence in a small plaque mutant of the infectious bursal disease virus

Cited by 33 publications

References 9 publications

Reversion of molecularly engineered, partially attenuated, very virulent infectious bursal disease virus during infection of commercial chickens

Reversion of molecularly engineered, partially attenuated, very virulent infectious bursal disease virus during infection of commercial chickens

A recombinant fowlpox virus that expresses the VP2 antigen of infectious bursal disease virus induces protection against mortality caused by the virus

Infectious bursal disease virus persistently infects bursal B-lymphoid DT40 cells

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