Increased virulence of an infectious bursal disease live virus vaccine after passage in chicks

Muskett, J.C.; Reed, N.E.; Thornton, Denise H.

doi:10.1016/s0264-410x(85)90161-6

Cited by 39 publications

(23 citation statements)

References 16 publications

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“…In some of the changes found in this study, the sequence peaks of the vv form were found to be a mixture of two peaks (Figure 2), raising the possibility that the two different forms exist in the viral population before attenuation, and following attenuation one population disappears. A similar explanation was given by Muskett et al (1985), who found an increase in the virulence of an attenuated strain following passages in susceptible birds. This was suggested to be due to the selection of a virulent subpopulation present in the vaccine.…”

Section: Discussionsupporting

confidence: 68%

Attenuation of very virulent infectious bursal disease virus and comparison of full sequences of virulent and attenuated strains

Lazarus

Pasmanik‐Chor

Gutter³

et al. 2008

Avian Pathology

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A very virulent strain of infectious bursal disease virus (IBDVks) was isolated from the bursae of Fabricius of IBDV-affected broiler chickens. Following 43 serial passages in specific pathogen-free embryonated eggs, an attenuated strain was established (IBDVmb). Dosages of IBDVmb in the range 10 2 to 10 4 embryo infective dose of 50% were found to be safe and protective for commercial chicks. Chickens vaccinated with live vaccine containing IBDVmb responded with precipitating and type-specific neutralizing antibodies, and were immune to subsequent challenge with a very virulent IBDV. IBDVmb has been used as an attenuated vaccine throughout the world since 1993. A comparison of the full sequences of the virulent and attenuated strains (IBDVks and IBDVmb, respectively) revealed seven nucleotides that were different, four of them leading to changes in the amino-acid sequence. Comparison of the protein sequencse of these strains and published sequences of very virulent and attenuated phenotypes lead us to sugget that the novel difference responsible for virulence of the Israeli strains are: residue 272 (VP2, very conserved site) and residue 527 (VP4), both in segment A, and in segment B (VP1) residues 96 and 161 (both conserved). Our study strengthens the possibility that more than one protein is involved in IBDV attenuation. In all reports, including ours, virulence was reduced without affecting antigenicity of the neutralizing epitopes in VP2. This could have practical implications for attenuated-vaccine development.

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Section: Discussionsupporting

confidence: 68%

Attenuation of very virulent infectious bursal disease virus and comparison of full sequences of virulent and attenuated strains

Lazarus

Pasmanik‐Chor

Gutter³

et al. 2008

Avian Pathology

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“…In vitro passage of IBDV has been associated with attenuation of virulence as it is a common approach for developing attenuated live vaccine strains (Skeeles & Lukert, 1980;Yamaguchi et al, 1996), whereas in vivo passage of the IBD vaccine strains has been associated with an increase in virulence (Muskett et al, 1985;Yamaguchi et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…In vitro passage of IBDV strains results in reduced pathogenicity in vivo (Hassan et al, 1996a;Yamaguchi et al, 1996). Conversely, in vivo passages of the attenuated viruses in susceptible chickens progressively revert to virulence (Muskett et al, 1985;Yamaguchi et al, 2000). This study was conducted to seek correlations between virulence and amino acid changes in the variable region of VP2 in a plaque-purified field IBDV, and its in vivopassaged and in vitro-passaged derivative viruses.…”

Section: Introductionmentioning

confidence: 99%

Amino acid changes in the variable region of VP2 in three infectious bursal disease viruses with different virulence, originating from a common ancestor

Toroghi¹,

Kataria²,

Verma³

et al. 2001

Avian Pathology

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“…There is good experimental evidence for a positive correlation between the reproduction rate and virulence for many parasites (Muskett et al 1985;Bull et al 1991;Bull and Molineux 1992;Ni and Kemp 1992;Ebert and Mangin 1997). Thus, we assume for the following that the reproduction rate of parasites is proportional to their virulences, that is c 1i ϭ p ϫ a 1i and c 2i ϭ p ϫ a 2i , where p is a constant of proportionality.…”

Section: Modelmentioning

confidence: 99%

Evolution of Virulence in a Heterogeneous Host Population

2000

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Abstract. There is a large body of theoretical studies that investigate factors that affect the evolution of virulence, that is parasite-induced host mortality. In these studies the host population is assumed to be genetically homogeneous. However, many parasites have a broad range of host types they infect, and trade-offs between the parasite virulence in different host types may exist. The aim of this paper is to study the effect of host heterogeneity on the evolution of parasite virulence. By analyzing a simple model that describes the replication of different parasite strains in a population of two different host types, we determine the optimal level of virulence in both host types and find the conditions under which strains that specialize in one host type dominate the parasite population. Furthermore, we show that intrahost evolution of the parasite during an infection may lead to stable polymorphisms and could introduce evolutionary branching in the parasite population.Key words. Evolution of virulence, genetic trade-offs, host heterogeneity, host-parasite coevolution, intrahost evolution, serial passage.Received December 31, 1998. Accepted July 16, 1999 The relationship between a parasite and its host is a story of benefits and harms. The parasite benefits from the host by living in and on it and by using host resources to reproduce. The parasite's benefit gives rise to the host's harm: The life span of the host is usually shortened by infection, and important fitness traits of the host, such as fecundity, are often negatively affected by the parasite (Ewald 1994). However, by reducing the life span or the fitness of its host, the parasite may inflict harm upon itself. The question emerges: What evolutionary forces determine the level of harm inflicted on the host? In this paper, we focus on the evolution of parasite virulence, here defined as parasite-induced host mortality.If virulence were an independent trait, natural selection should favor parasites with low virulence. A parasite that does not kill its host has more time to exploit it and to be transmitted, thus increasing its own fitness. Therefore, in the long run the parasite should evolve to be avirulent. Nevertheless, there are many examples of intermediately or highly virulent host-parasite systems with a long coevolutionary history (Fenner and Ratcliffe 1965;Herre 1993). To account for virulent host-parasite interactions, trade-offs between virulence and other parasite traits such as infectivity, transmissibility, or reproduction rate were postulated , 1982, 1991May and Anderson 1979, 1983, 1990Levin and Pimentel 1981;Bremermann and Pickering 1983;Ewald 1983;Knolle 1989; Frank 1992;Antia et al. 1994). Furthermore, it was argued that in systems in which the parasite can super-or coinfect hosts or in which the parasites frequently generate new mutant strains within a host, a parasite strain with high virulence may have a competitive advantage over less virulent strains within the host (Hamilton 1972;Bremermann and Pickering 1983;Knolle 1989;Sas...

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Increased virulence of an infectious bursal disease live virus vaccine after passage in chicks

Cited by 39 publications

References 16 publications

Attenuation of very virulent infectious bursal disease virus and comparison of full sequences of virulent and attenuated strains

Attenuation of very virulent infectious bursal disease virus and comparison of full sequences of virulent and attenuated strains

Amino acid changes in the variable region of VP2 in three infectious bursal disease viruses with different virulence, originating from a common ancestor

Evolution of Virulence in a Heterogeneous Host Population

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