Summary auto-generated
This study investigates why pathogenic serotype 1 IBDV replicates efficiently in bursal lymphoid cells while apathogenic serotype 2 strains do not. Researchers compared virus binding patterns across chicken lymphoid cells (bursa, spleen, thymus) and chicken embryo fibroblasts (CEF) using radiolabeled virus particles, saturation assays, and competition experiments. Both IBDV serotypes bound to all cell types tested, but with notable differences: serotype 2 bound extensively to lymphoid cells, while serotype 1 showed minimal binding despite efficient replication in bursal cells. Using virus overlay proteome binding assays (VOPBA), researchers identified common receptor proteins of 40 kDa and 46 kDa present on all cell types. These findings demonstrate that differential viral replication is not determined by receptor availability alone, as lymphoid cells possess binding sites for both serotypes yet remain non-permissive for serotype 1. The presence of serotype-specific binding sites varied between cell types and serotypes, suggesting that post-binding cellular factors, rather than initial virus attachment, determine host cell tropism and pathogenicity of IBDV strains.
Key findings
- Both IBDV serotypes bind to lymphoid cells and CEF, but serotype 1 binds poorly to lymphoid cells despite replicating efficiently in bursal tissue
- Virus-cell tropism differences are not explained by presence or absence of specific receptor binding sites
- The 40 kDa and 46 kDa cell surface proteins serve as common attachment sites for both IBDV serotypes across all cell types tested
- Post-binding cellular factors, not initial receptor availability, likely determine whether IBDV can replicate in different lymphoid cell populations
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Abstract
Institut für Virologie, Justus-Liebig-Universität Giessen, Frankfurter Strasse 107, D-35392, Giessen and Institut für Virologie, Universität Leipzig,,† Margarete-Blank-Strasse 8, D-04103 Leipzig, Germany
Pathogenic serotype 1 strains of infectious bursal disease virus (IBDV) replicate efficiently in lymphoid cells of the bursa of Fabricius of chicken. Lymphoid cells in other organs are not susceptible. Apathogenic serotype 2 strains do not replicate in lymphoid bursa cells or in other lymphoid cells. Chicken embryo fibroblasts (CEF), however, efficiently replicate strains of either serotype. Binding studies showed that strains of both IBDV serotypes bind to lymphoid cells isolated from the bursa, thymus or spleen, indicating that restriction of IBDV replication to lymphoid B cells is not determined by the presence of specific receptor sites. The specificity of binding was demonstrated by saturation and competition experiments. These revealed the presence of different receptors: CEF had receptors common to both serotypes and specific ones for each serotype. Receptor sites common to both serotypes were also present on lymphoid cells; however, additional serotype-specific sites were only demonstrated for the apathogenic serotype 2 strain. Strains of both serotypes specificially bound to proteins with molecular masses of 40 kDa and 46 kDa, exposed on the surface of CEF and lymphoid cells. Competition experiments indicated that these proteins might represent the common receptor sites of IBDV.