Pathogenicity of the novel antigenic variant infectious bursal disease virus B2977CE2C3 isolated in Japan: Histological analysis of experimentally infected chickens.

Abstract

Infectious bursal disease (IBD) is an immunosuppressive disease caused by the IBD virus (IBDV), leading to substantial economic losses in the poultry industry. Recently, a novel antigenic variant IBDV (nvIBDV) has emerged in China and spread across Asia, including Japan. We previously isolated and characterized the nvIBDV strain, B2977CE2C3, by experimentally infecting specific pathogen-free chickens. Herein, we performed histological examinations of systemic organs using tissue samples from the infected chickens. At 3 days post-inoculation (dpi), lymphocyte depletion was observed in the bursa of Fabricius (BF), cecal tonsil, spleen, and thymic cortex. During the acute phase, the BF exhibited marked inflammation and accumulation of cell debris, likely apoptotic remnants. Immunohistochemistry and quantitative image analysis revealed significant B cell depletion in the BF and spleen, persisting for up to 21 dpi. In addition, structural destruction of the BF, including loss of follicles, epithelial infoldings, replacement by epithelial reticular cells, and stromal fibrosis, was observed. IBDV antigens were immunohistochemically detected in the BF and cecal tonsil during early infection. The bone marrow contained lymphoid cell aggregations, suggesting increased lymphopoiesis. These findings indicate that the pathogenicity of nvIBDV is comparable with that of classical IBDV (genogroup A1), although it belongs to genogroup A2. Notably, nvIBDV can induce chronic immunosuppression due to prolonged B cell depletion in the BF and spleen, thereby increasing the susceptibility to secondary infections and interfering with subsequent vaccinations. This study highlights the pathogenic potential of nvIBDV and provides valuable pathological insights for understanding its pathogenesis and evaluating preventive strategies.