Recombinant GI-19 infectious bronchitis virus induction of humoral immunosuppression with reduced HI antibody response following Newcastle disease virus vaccination and bursal cell apoptosis

Abstract Pathological changes and viral presence in the bursa of Fabricius (BF) have been reported, but the immunosuppression of infectious bronchitis virus (IBV) remains poorly characterized. Here, we systematically evaluated the pathogenicity of two GI-19 lineage IBV isolates, CK/CH/FJ-B3/2023 (bursal origin) and CK/CH/FJ-T5/2023 (tracheal origin), in 7-day-old specific pathogen-free (SPF) chicks, including further assessments of serum cytokines and the bursal apoptosis. We further assessed the impacts of these two IBV isolates on the Newcastle disease virus (NDV) inactivated vaccine-induced hemagglutination inhibition (HI) antibody response. This study reveals that both GI-19 lineage IBV isolates, which originated from the recombination of the 4/91 vaccine strain, exhibit bursa-tropism, inducing bursal pathological atrophy, prolonged viral detection [up to 35 days post-infection (dpi)] and delayed seroconversion until 14 dpi. Notably, IBV infection induces humoral immunosuppression in SPF chickens, evidenced by a ≥ 1log 2 reduction in NDV-HI antibody titers at 14 and 28 dpi, with antibody production recovering to normal levels by 35 dpi. This is accompanied by a sustained systemic proinflammatory response characterized by persistent upregulation of tumor necrosis factor- α (TNF- α ), interleukin 1 β (IL-1 β ), IL-6, and interferon-gamma (IFN- γ ) in the serum of infected chicks up to 28 dpi. Early-onset bursal apoptosis was detected as early as 1 dpi, with the bursal apoptosis index significantly higher than that of the negative control throughout the observation period. These findings highlight the humoral immunosuppression induced by IBV variants. Further characterization of IBV types is warranted to elucidate IBV immunosuppressive mechanisms.