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Recently, the identification of novel reassortants of infectious bursal disease (IBD) virus (IBDV) was reported. Interestingly, these strains competed with the previously dominant A3B2 lineage, becoming the prevalent lineage in Poland and disseminating to other countries in Europe. However, the specific virulence properties that facilitate their spreading were not elucidated. In this study, we compared the pathogenesis of the A3B4 Bug/03 and A3B2 75/11 IBDV strains in specific-pathogen-free (SPF) chickens, integrating viral replication dynamics, tissue tropism, immunosuppressive effects and host transcriptional responses. Both strains replicated efficiently in lymphoid and non-lymphoid tissues, with peak viral loads in the bursa of Fabricius. While the A3B2 75/11 strain exhibited higher viral RNA levels at early time points, the A3B4 Bug/03 strain persisted longer in multiple tissues. Notably, the A3B4 Bug/03 strain induced earlier bursal atrophy despite comparable viral loads at 4 dpi, and was associated with heterogeneous growth performance, reflecting uneven flock development. Transcriptomic analysis revealed distinct host response profiles between strains. Infection with the A3B4 virus was characterised by the enrichment of metabolic and translational pathways, indicating cellular adaptation and metabolic reprogramming. In contrast, the A3B2 75/11 strain triggered a strong activation of immune and inflammatory pathways, including cytokine and chemokine signalling. Collectively, these findings demonstrate that IBDV pathogenicity is not solely determined by viral replication, but is critically shaped by host response mechanisms. The ability of A3B4 strains to modulate host pathways and persist in infected birds likely contributes to their epidemiological success and facilitates their continued spread in poultry populations.
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Pikuła et al. (2026) studied this question.
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